Parties involved in these conflicts include locally affected
communities, states, companies and investors, and social or
environmental movements; typically environmental defenders are protecting their homelands from resource extraction or hazardous waste disposal. Resource extraction and hazardous waste activities often create resource scarcities (such as by overfishing or deforestation), pollute the environment, and degrade the living space for humans and nature, resulting in conflict. A particular case of environmental conflicts are forestry conflicts, or forest conflicts
which "are broadly viewed as struggles of varying intensity between
interest groups, over values and issues related to forest policy and the
use of forest resources". In the last decades, a growing number of these have been identified globally.
Frequently environmental conflicts focus on environmental justice issues, the rights of indigenous people, the rights of peasants, or threats to communities whose livelihoods are dependent on the ocean.
Outcomes of local conflicts are increasingly influenced by
trans-national environmental justice networks that comprise the global
environmental justice movement.
Environmental conflict can complicate response to natural disaster or exacerbate existing conflicts – especially in the context of geopolitical disputes or where communities have been displaced to create environmental migrants. The study of these conflicts is related to the fields of ecological economics, political ecology, and environmental justice.
Causes
The
origin of environmental conflicts can be directly linked to the
industrial economy. As less than 10% of materials and energy are
recycled, the industrial economy is constantly expanding energy and
material extraction at commodity frontiers through two main processes:
Appropriating new natural resources through territorial claims and land grabs.
Making exploitation of existing sites more efficient through investments or social and technical innovation.
EDCs are caused by the unfair distribution
of environmental costs and benefits. These conflicts arise from social
inequality, contested claims over territory, the proliferation of
extractive industries, and the impacts of the economic industrialization
over the past centuries. Oil, mining, and agriculture industries are
focal points of environmental conflicts.
Types of conflicts
Environmental defenders use a wide range of tacticsMost environmental conflicts are in the mining, energy, and waste disposal sectors.
A 2020 paper mapped the arguments and concerns of environmental defenders in over 2743 conflicts found in the Environmental Justice Atlas (EJAtlas). The analysis found that the industrial sectors most frequently challenged by environmental conflicts were mining (21%), fossil energy (17%), biomass and land uses (15%), and water management (14%). Killings of environmental defenders happened in 13% of the reported cases.
There was also a distinct difference in the types of conflict
found in high and low income countries. There were more conflicts around
conservation, water management, and biomass and land use in low income
countries; while in high income countries almost half of conflicts
focused on waste management, tourism, nuclear power, industrial zones, and other infrastructure projects.
The study also found that most conflicts start with self-organized
local groups defending against infringement, with a focus on non-violent
tactics.
Environmental conflicts can be classified based on the different stages of the commodity
chain: during the extraction of energy sources or materials, in the
transportation and production of goods, or at the final disposal of
waste.
EJAtlas Categories
The
EJAtlas was founded and is co-directed by Leah Temper and Joan
Martinez-Alier, and it is coordinated by Daniela Del Bene. Its aim is
“to document, understand and analyse the political outcomes that emerge
or that may emerge” from ecological distribution conflicts. It is housed at the ICTA of the Universitat Autonoma de Barcelona. Since 2012, academics and activists have collaborated to write the entries, reaching 3,500 by July 2021.
The EJ Atlas identifies ten categories of ecological distribution conflicts:
Biodiversity conservation conflicts:
Biomass and land conflicts (Forests, Agriculture, Fisheries and Livestock Management)
Fossil Fuels and Climate Justice/Energy
Industrial and Utilities Conflicts
Infrastructure and Built Environment
Mineral Ores and Building Materials Extraction
Nuclear
Tourism Recreation
Waste Management
Water Management
Ecological distribution conflicts
Ecological Distribution Conflicts (EDCs) were introduced as a concept in 1995 by Joan Martínez-Alier and Martin O'Connor
to facilitate more systematic documentation and analysis of
environmental conflicts and to produce a more coherent body of academic,
activist, and legal work around them.
EDCs arise from the unfair access to natural resources, unequally
distributed burdens of environmental pollution, and relate to the
exercise of power by different social actors when they enter into
disputes over access to or impacts on natural resources. For example, a
factory may pollute a river thus affecting the community whose
livelihood depends on the water of the river. The same can apply to the
climate crisis, which may cause sea level rise on some Pacific islands.
This type of damage is often not valued by the market, preventing those affected from being compensated.
Ecological conflicts occur at both global and local scales. Often
conflicts take place between the global South and the global North,
e.g. a Finnish forest company operating in Indonesia, or in econonomic peripheries, although there is a growing emergence of conflicts in Europe,
including violent ones. There are also local conflicts that occur
within a short commodity chain (e.g. local extraction of sand and gravel
for a nearby cement factory).
Intellectual history
Since its conception, the term Ecological Distribution Conflict has been linked to research from the fields of political ecology, ecological economics, and ecofeminism. It has also been adopted into a non-academic setting through the environmental justice movement, where it branches academia and activism to assist social movements in legal struggles.
In his 1874 lecture ‘Wage Labour and Capital’, Karl Marx introduced the idea that economic relations under capitalism are inherently exploitative, meaning economic inequality is an inevitability of the system. He theorised that this is because capitalism expands through capital accumulation, an ever-increasing process which requires the economic subjugation of parts of the population in order to function.
Building on this theory, academics in the field of political
economy created the term ‘economic distribution conflicts’ to describe
the conflicts that occur from this inherent economic inequality. This type of conflict typically occurs between parties with an economic
relationship but unequal power dynamic, such as buyers and sellers, or
debtors and creditors.
However, Martinez Allier and Martin O’Connor noticed that this
term focuses solely on the economy, omitting the conflicts that do not
occur from economic inequality but from the unequal distribution of
environmental resources.
In response, in 1995, they coined the term ‘ecological distribution
conflict’. This type of conflict occurs at commodity frontiers, which
are constantly being moved and reframed due to society's unsustainable social metabolism.
These conflicts might occur between extractive industries and
Indigenous populations, or between polluting actors and those living on
marginalised land. Its roots can still be seen in Marxian theory, as it
is based on the idea that capitalism's need for expansion drives
inequality and conflict.
Unfair ecological distribution can be attributed to capitalism as a system of cost-shifting.
Neoclassical economics usually consider these impacts as “market
failures” or “externalities” that can be valued in monetary terms and
internalized into the price system. Ecological economics and political
ecology scholars oppose the idea of economic commensuration that could
form the basis of eco-compensation mechanisms for impacted communities. Instead, they advocate for different valuation languages such as sacredness, livelihood, rights of nature, Indigenous territorial rights, archaeological values, and ecological or aesthetic value.
Social movements
Ecological
distribution conflicts have given rise to many environmental justice
movements around the globe. Environmental justice scholars conclude that
these conflicts are a force for sustainability.These scholars study the dynamics that drive these conflicts towards an environmental justice success or a failure.
Globally, around 17% of all environmental conflicts registered in
the EJAtlas report environmental justices 'successes', such as stopping
an unsustainable project or redistributing resources in a more
egalitarian way.
Movements usually shape their repertoires of contention as protest forms and direct actions, which are influenced by national and local backgrounds.
In environmental justice struggles, the biophysical characteristics of
the conflict can further shape the forms of mobilization and direct
action. Resistance strategies can take advantage of ‘biophysical
opportunity structures’, where they attempt to identify, change or
disrupt the damaging ecological processes they are confronting.
Finally, the ‘collective action frames’
of movements emerging in response to environmental conflicts becomes
very powerful when they challenge the mainstream relationship of human
societies with the environment.
These frames are often expressed through pithy protest slogans, that
scholars refer to as the ‘vocabulary of environmental justice’ and which
includes concepts and phrases such as ‘environmental racism’, ‘tree
plantations are not forests’, ‘keep the oil in the soil’, ‘keep the coal
in the hole’ and the like, resonating and empathizing with those
communities affected by EDC.
Environmentalism of the poor
Some scholars make a distinction between environmentalist conflicts
that have an objective of sustainability or resource conservation and
environmental conflicts more broadly (which are any conflict over a
natural resource). The former type of conflict gives rise to environmentalism of the poor,
in which environmental defenders protect their land from degradation by
industrial economic forces. Environmentalist conflicts tend to be intermodal conflicts in which peasant or agricultural land uses are in conflict with industrial uses (such as mining). Intramodal conflicts, in which peasants dispute amongst themselves about land use may not be environmentalist.
In this division movement such as La Via Campesina (LVC), or the
International Planning Committee for Food Sovereignty (IPC) can be
considered in the halfway between these two approaches. In their defense
of peasant agriculture and against large-scale capitalist industrial
agriculture, both LVC and the IPC have fundamentally contributed to
promoting agroecology as a sustainable agriculture model across the
globe, adopting an intermodal approach against industrial agriculture
and providing new sources of education to poor communities that could
incentive an aware integration in the redistribution of resources.
A similar attitude has shaped the action of the Brazilian Landless
Farmworkers movement (MST) in the way it has struggled with the idea of
productivity and the use of chemical products by several agribusiness realities that destroy resources rich in fertility and biodiversity.
Such movements often question the dominant form of valuation of
resource uses (i.e. monetary values and cost-benefit analyses) and
renegotiate the values deemed relevant for sustainability.
Sometimes, particularly when the resistance weakens, demands for
monetary compensation are made (in a framework of ‘weak
sustainability’).
The same groups, at other times or when feeling stronger, might argue
in terms of values which are not commensurate with money, such as
indigenous territorial rights, irreversible ecological values, human
right to health or the sacredness of redefining the very economic,
ecological and social principles behind particular uses of the Mother
Earth, implicitly defending a conception of ‘strong sustainability’. In
contesting and environment, such intermodal conflicts are those that are
most clearly forced towards broader sustainability transitions.
Conflict resolution
A distinct field of conflict resolution called Environmental Conflict Resolution, focuses on developing collaborative methods for deescalating and resolving environmental conflicts.
As a field of practice, people working on conflict resolution focus on
the collaboration, and consensus building among stakeholders.
An analysis of such resolution processes found that the best predictor
of successful resolution was sufficient consultation with all parties
involved.
A new tool with certain potential in this regard is the
development of video games proposing distinct options to the gamers for
handling conflicts over environmental resources, for instance in the
fishery sector.
Critique
Some scholars critique the focus on natural resources used in descriptions of environmental conflict.
Often these approaches focus on the commercialization of the natural
environment that doesn't acknowledge the underlying value of a healthy environment.
In contrast to necrosis,
which is a form of traumatic cell death that results from acute
cellular injury, apoptosis is a highly regulated and controlled process
that confers advantages during an organism's life cycle. For example,
the separation of fingers and toes in a developing human embryo occurs because cells between the digits undergo apoptosis. Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them.
Because apoptosis cannot stop once it has begun, it is a highly
regulated process. Apoptosis can be initiated through one of two
pathways. In the intrinsic pathway the cell kills itself because it senses cell stress, while in the extrinsic pathway
the cell kills itself because of signals from other cells. Weak
external signals may also activate the intrinsic pathway of apoptosis. Both pathways induce cell death by activating caspases, which are proteases,
or enzymes that degrade proteins. The two pathways both activate
initiator caspases, which then activate executioner caspases, which then
kill the cell by degrading proteins indiscriminately.
In addition to its importance as a biological phenomenon,
defective apoptotic processes have been implicated in a wide variety of
diseases. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer. Some factors like Fas receptors and caspases promote apoptosis, while some members of the Bcl-2 family of proteins inhibit apoptosis.
German scientist Carl Vogt was first to describe the principle of apoptosis in 1842. In 1885, anatomist Walther Flemming
delivered a more precise description of the process of programmed cell
death. However, it was not until 1965 that the topic was resurrected.
While studying tissues using electron microscopy, John Kerr at the University of Queensland was able to distinguish apoptosis from traumatic cell death. Following the publication of a paper describing the phenomenon, Kerr was invited to join Alastair Currie, as well as Andrew Wyllie, who was Currie's graduate student, at the University of Aberdeen. In 1972, the trio published a seminal article in the British Journal of Cancer. Kerr had initially used the term programmed cell necrosis, but in the article, the process of natural cell death was called apoptosis.
Kerr, Wyllie and Currie credited James Cormack, a professor of Greek
language at University of Aberdeen, with suggesting the term apoptosis.
Kerr received the Paul Ehrlich and Ludwig Darmstaedter Prize on March 14, 2000, for his description of apoptosis. He shared the prize with Boston biologist H. Robert Horvitz.
For many years, neither "apoptosis" nor "programmed cell death"
was a highly cited term. Two discoveries brought cell death from
obscurity to a major field of research: identification of the first
component of the cell death control and effector mechanisms, and linkage
of abnormalities in cell death to human disease, in particular cancer.
This occurred in 1988 when it was shown that BCL2, the gene responsible
for follicular lymphoma, encoded a protein that inhibited cell death.
In Greek, apoptosis translates to the "falling off" of leaves from a tree.
Cormack, professor of Greek language, reintroduced the term for medical
use as it had a medical meaning for the Greeks over two thousand years
before. Hippocrates used the term to mean "the falling off of the bones". Galen
extended its meaning to "the dropping of the scabs". Cormack was no
doubt aware of this usage when he suggested the name. Debate continues
over the correct pronunciation, with opinion divided between a
pronunciation with the second p silent (/æpəˈtoʊsɪs/ap-ə-TOH-sis) and the second p pronounced (/eɪpəpˈtoʊsɪs/). In English, the p of the Greek -pt-consonant cluster is typically silent at the beginning of a word (e.g. pterodactyl, Ptolemy), but articulated when used in combining forms preceded by a vowel, as in helicopter or the orders of insects: diptera, lepidoptera, etc.
In the original Kerr, Wyllie & Currie paper, there is a footnote regarding the pronunciation:
We are most grateful to Professor James Cormack of the
Department of Greek, University of Aberdeen, for suggesting this term.
The word "apoptosis" (ἀπόπτωσις)
is used in Greek to describe the "dropping off" or "falling off" of
petals from flowers, or leaves from trees. To show the derivation
clearly, we propose that the stress should be on the penultimate
syllable, the second half of the word being pronounced like "ptosis"
(with the "p" silent), which comes from the same root "to fall", and is
already used to describe the drooping of the upper eyelid.
Activation mechanisms
Control of the apoptotic mechanisms
The initiation of apoptosis is tightly regulated by activation
mechanisms, because once apoptosis has begun, it inevitably leads to the
death of the cell. The two best-understood activation mechanisms are the intrinsic pathway (also called the mitochondrial pathway) and the extrinsic pathway. The intrinsic pathway
is activated by intracellular signals generated when cells are stressed
and depends on the release of proteins from the intermembrane space of
mitochondria. The extrinsic pathway is activated by extracellular ligands binding to cell-surface death receptors, which leads to the formation of the death-inducing signaling complex (DISC).
A cell initiates intracellular apoptotic signaling in response to a stress, which may bring about cell suicide. The binding of nuclear receptors by glucocorticoids, heat, radiation, nutrient deprivation, viral infection, hypoxia, increased intracellular concentration of free fatty acids and increased intracellular calcium concentration,
for example, by damage to the membrane, can all trigger the release of
intracellular apoptotic signals by a damaged cell. A number of cellular
components, such as poly ADP ribose polymerase, may also help regulate apoptosis. Single cell fluctuations have been observed in experimental studies of stress induced apoptosis.
Before the actual process of cell death is precipitated by
enzymes, apoptotic signals must cause regulatory proteins to initiate
the apoptosis pathway. This step allows those signals to cause cell
death, or the process to be stopped, should the cell no longer need to
die. Several proteins are involved, but two main methods of regulation
have been identified: the targeting of mitochondria functionality, or directly transducing the signal via adaptor proteins
to the apoptotic mechanisms. An extrinsic pathway for initiation
identified in several toxin studies is an increase in calcium
concentration within a cell caused by drug activity, which also can
cause apoptosis via a calcium binding protease calpain.
Intrinsic pathway
The intrinsic pathway is also known as the mitochondrial pathway. Mitochondria are essential to multicellular life. Without them, a cell ceases to respire aerobically
and quickly dies. This fact forms the basis for some apoptotic
pathways. Apoptotic proteins that target mitochondria affect them in
different ways. They may cause mitochondrial swelling through the
formation of membrane pores, or they may increase the permeability of
the mitochondrial membrane and cause apoptotic effectors to leak out. There is also a growing body of evidence indicating that nitric oxide is able to induce apoptosis by helping to dissipate the membrane potential of mitochondria and therefore make it more permeable.
Nitric oxide has been implicated in initiating and inhibiting apoptosis
through its possible action as a signal molecule of subsequent pathways
that activate apoptosis.
During apoptosis, cytochrome c is released from mitochondria through the actions of the proteins Bax and Bak.
The mechanism of this release is enigmatic, but appears to stem from a
multitude of Bax/Bak homo- and hetero-dimers of Bax/Bak inserted into
the outer membrane. Once cytochrome c is released it binds with Apoptotic protease activating factor – 1 (Apaf-1) and ATP, which then bind to pro-caspase-9 to create a protein complex known as an apoptosome. The apoptosome cleaves the pro-caspase to its active form of caspase-9, which in turn cleaves and activates pro-caspase into the effector caspase-3.
Mitochondria also release proteins known as SMACs (second mitochondria-derived activator of caspases) into the cell's cytosol following the increase in permeability of the mitochondria membranes. SMAC binds to proteins that inhibit apoptosis
(IAPs) thereby deactivating them, and preventing the IAPs from
arresting the process and therefore allowing apoptosis to proceed. IAP
also normally suppresses the activity of a group of cysteine proteases called caspases,
which carry out the degradation of the cell. Therefore, the actual
degradation enzymes can be seen to be indirectly regulated by
mitochondrial permeability.
Extrinsic pathway
Overview of signal transduction pathways
Overview of TNF (left) and Fas (right) signalling in apoptosis, an example of direct signal transduction
Two theories of the direct initiation of apoptotic mechanisms in mammals have been suggested: the TNF-induced (tumor necrosis factor) model and the Fas-Fas ligand-mediated model, both involving receptors of the TNF receptor (TNFR) family coupled to extrinsic signals.
TNF pathway
TNF-alpha is a cytokine produced mainly by activated macrophages, and is the major extrinsic mediator of apoptosis. Most cells in the human body have two receptors for TNF-alpha: TNFR1 and TNFR2.
The binding of TNF-alpha to TNFR1 has been shown to initiate the
pathway that leads to caspase activation via the intermediate membrane
proteins TNF receptor-associated death domain (TRADD) and Fas-associated death domain protein (FADD). cIAP1/2 can inhibit TNF-α signaling by binding to TRAF2. FLIP inhibits the activation of caspase-8. Binding of this receptor can also indirectly lead to the activation of transcription factors involved in cell survival and inflammatory responses. However, signalling through TNFR1 might also induce apoptosis in a caspase-independent manner.
The link between TNF-alpha and apoptosis shows why an abnormal
production of TNF-alpha plays a fundamental role in several human
diseases, especially in autoimmune diseases. The TNF-alpha receptor superfamily also includes death receptors (DRs), such as DR4 and DR5. These receptors bind to the protein TRAIL and mediate apoptosis. Apoptosis is known to be one of the primary mechanisms of targeted cancer therapy.
Luminescent iridium complex-peptide hybrids (IPHs) have recently been
designed, which mimic TRAIL and bind to death receptors on cancer cells,
thereby inducing their apoptosis.
The fas receptor (First apoptosis signal) – (also known as Apo-1 or CD95) is a transmembrane protein of the TNF family which binds the Fas ligand (FasL). The interaction between Fas and FasL results in the formation of the death-inducing signaling complex
(DISC), which contains the FADD, caspase-8 and caspase-10. In some
types of cells (type I), processed caspase-8 directly activates other
members of the caspase family, and triggers the execution of apoptosis
of the cell. In other types of cells (type II), the Fas-DISC
starts a feedback loop that spirals into increasing release of
proapoptotic factors from mitochondria and the amplified activation of
caspase-8.[41]
Common components
Following TNF-R1 and Fas activation in mammalian cells a balance between proapoptotic (BAX, BID, BAK, or BAD) and anti-apoptotic (Bcl-Xl and Bcl-2) members of the Bcl-2 family are established. This balance is the proportion of proapoptotic homodimers
that form in the outer-membrane of the mitochondrion. The proapoptotic
homodimers are required to make the mitochondrial membrane permeable for
the release of caspase activators such as cytochrome c and SMAC.
Control of proapoptotic proteins under normal cell conditions of
nonapoptotic cells is incompletely understood, but in general, Bax or
Bak are activated by the activation of BH3-only proteins, part of the Bcl-2 family.
Caspases
Caspases
play the central role in the transduction of ER apoptotic signals.
Caspases are proteins that are highly conserved, cysteine-dependent
aspartate-specific proteases. There are two types of caspases: initiator
caspases (caspases 2, 8, 9, 10, 11, and 12) and effector caspases
(caspases 3, 6, and 7). The activation of initiator caspases requires
binding to specific oligomeric activator protein. Effector caspases are then activated by these active initiator caspases through proteolytic
cleavage. The active effector caspases then proteolytically degrade a
host of intracellular proteins to carry out the cell death program.
Caspase-independent apoptotic pathway
There also exists a caspase-independent apoptotic pathway that is mediated by AIF (apoptosis-inducing factor).
Apoptosis model in amphibians
The frog Xenopus laevis
serves as an ideal model system for the study of the mechanisms of
apoptosis. In fact, iodine and thyroxine also stimulate the spectacular
apoptosis of the cells of the larval gills, tail and fins in amphibian's
metamorphosis, and stimulate the evolution of their nervous system
transforming the aquatic, vegetarian tadpole into the terrestrial,
carnivorous frog.
Negative regulators of apoptosis
Negative regulation of apoptosis inhibits cell death signaling pathways, helping tumors to evade cell death and developing drug resistance. The ratio between anti-apoptotic (Bcl-2) and pro-apoptotic (Bax) proteins determines whether a cell lives or dies. Many families of proteins act as negative regulators categorized into either antiapoptotic factors, such as IAPs and Bcl-2 proteins or prosurvival factors like cFLIP, BNIP3, FADD, Akt, and NF-κB.
Proteolytic caspase cascade: Killing the cell
Many
pathways and signals lead to apoptosis, but these converge on a single
mechanism that actually causes the death of the cell. After a cell
receives stimulus, it undergoes organized degradation of cellular
organelles by activated proteolytic caspases. In addition to the destruction of cellular organelles, mRNA is rapidly and globally degraded by a mechanism that is not yet fully characterized. mRNA decay is triggered very early in apoptosis.
A cell undergoing apoptosis shows a series of characteristic morphological changes. Early alterations include:
Cell shrinkage and rounding occur because of the retraction of lamellipodia and the breakdown of the proteinaceous cytoskeleton by caspases.
The cytoplasm appears dense, and the organelles appear tightly packed.
Chromatin undergoes condensation into compact patches against the nuclear envelope (also known as the perinuclear envelope) in a process known as pyknosis, a hallmark of apoptosis.
The nuclear envelope becomes discontinuous and the DNA inside it is fragmented in a process referred to as karyorrhexis. The nucleus breaks into several discrete chromatin bodies or nucleosomal units due to the degradation of DNA.
Apoptosis progresses quickly and its products are quickly removed,
making it difficult to detect or visualize on classical histology
sections. During karyorrhexis, endonuclease activation leaves short DNA fragments, regularly spaced in size. These give a characteristic "laddered" appearance on agar gel after electrophoresis. Tests for DNA laddering differentiate apoptosis from ischemic or toxic cell death.
Apoptotic cell disassembly
Different steps in apoptotic cell disassembly
Before the apoptotic cell is disposed of, there is a process of
disassembly. There are three recognized steps in apoptotic cell
disassembly:
Membrane blebbing: The cell membrane shows irregular buds known as blebs. Initially these are smaller surface blebs. Later these can grow into larger so-called dynamic membrane blebs. An important regulator of apoptotic cell membrane blebbing is ROCK1 (rho associated coiled-coil-containing protein kinase 1).
Formation of membrane protrusions: Some cell types, under specific
conditions, may develop different types of long, thin extensions of the
cell membrane called membrane protrusions. Three types have been
described: microtubule spikes, apoptopodia (feet of death), and beaded apoptopodia (the latter having a beads-on-a-string appearance). Pannexin 1 is an important component of membrane channels involved in the formation of apoptopodia and beaded apoptopodia.
Fragmentation: The cell breaks apart into multiple vesicles called apoptotic bodies, which undergo phagocytosis. The plasma membrane protrusions may help bring apoptotic bodies closer to phagocytes.
Removal of dead cells
The removal of dead cells by neighboring phagocytic cells has been termed efferocytosis.
Dying cells that undergo the final stages of apoptosis display phagocytotic molecules, such as phosphatidylserine, on their cell surface.
Phosphatidylserine is normally found on the inner leaflet surface of
the plasma membrane, but is redistributed during apoptosis to the
extracellular surface by a protein known as scramblase. These molecules mark the cell for phagocytosis by cells possessing the appropriate receptors, such as macrophages. The removal of dying cells by phagocytes occurs in an orderly manner without eliciting an inflammatory response.
During apoptosis cellular RNA and DNA are separated from each other and
sorted to different apoptotic bodies; separation of RNA is initiated as
nucleolar segregation.
Pathway knock-outs
Many knock-outs have been made in the apoptosis pathways to test the function of each of the proteins. Several caspases, in addition to APAF1 and FADD,
have been mutated to determine the new phenotype. In order to create a
tumor necrosis factor (TNF) knockout, an exon containing the
nucleotides 3704–5364 was removed from the gene.
This exon encodes a portion of the mature TNF domain, as well as the
leader sequence, which is a highly conserved region necessary for proper
intracellular processing. TNF-/- mice develop normally and have no
gross structural or morphological abnormalities. However, upon
immunization with SRBC (sheep red blood cells), these mice demonstrated a
deficiency in the maturation of an antibody response; they were able to
generate normal levels of IgM, but could not develop specific IgG
levels. Apaf-1 is the protein that turns on caspase 9 by cleavage to begin the caspase cascade that leads to apoptosis.
Since a -/- mutation in the APAF-1 gene is embryonic lethal, a gene
trap strategy was used in order to generate an APAF-1 -/- mouse. This
assay is used to disrupt gene function by creating an intragenic gene
fusion. When an APAF-1 gene trap is introduced into cells, many
morphological changes occur, such as spina bifida, the persistence of
interdigital webs, and open brain.
In addition, after embryonic day 12.5, the brain of the embryos showed
several structural changes. APAF-1 cells are protected from apoptosis
stimuli such as irradiation. A BAX-1 knock-out mouse exhibits normal
forebrain formation and a decreased programmed cell death in some
neuronal populations and in the spinal cord, leading to an increase in
motor neurons.
The caspase proteins are integral parts of the apoptosis pathway,
so it follows that knock-outs made have varying damaging results. A
caspase 9 knock-out leads to a severe brain malformation . A caspase 8 knock-out leads to cardiac failure and thus embryonic lethality .
However, with the use of cre-lox technology, a caspase 8 knock-out has
been created that exhibits an increase in peripheral T cells, an
impaired T cell response, and a defect in neural tube closure.
These mice were found to be resistant to apoptosis mediated by CD95,
TNFR, etc. but not resistant to apoptosis caused by UV irradiation,
chemotherapeutic drugs, and other stimuli. Finally, a caspase 3
knock-out was characterized by ectopic cell masses in the brain and
abnormal apoptotic features such as membrane blebbing or nuclear
fragmentation.
A remarkable feature of these KO mice is that they have a very
restricted phenotype: Casp3, 9, APAF-1 KO mice have deformations of
neural tissue and FADD and Casp 8 KO showed defective heart development,
however, in both types of KO other organs developed normally and some
cell types were still sensitive to apoptotic stimuli suggesting that
unknown proapoptotic pathways exist.
Methods for distinguishing apoptotic from necrotic cells
Long-term
live cell imaging (12h) of multinucleated mouse pre-Adipocyte trying to
undergo mitosis. Due to the excess of genetic material the cell fails
to replicate and dies by apoptosis.
Label-free live cell imaging, time-lapse microscopy, flow fluorocytometry, and transmission electron microscopy
can be used to compare apoptotic and necrotic cells. There are also
various biochemical techniques for analysis of cell surface markers
(phosphatidylserine exposure versus cell permeability by flow
cytometry), cellular markers such as DNA fragmentation (flow cytometry), caspase activation, Bid cleavage, and cytochrome c release (Western blotting).
Supernatant screening for caspases, HMGB1, and cytokeratin 18 release
can identify primary from secondary necrotic cells. However, no distinct
surface or biochemical markers of necrotic cell death have been
identified yet, and only negative markers are available. These include
absence of apoptotic markers (caspase activation, cytochrome c release,
and oligonucleosomal DNA fragmentation) and differential kinetics of
cell death markers (phosphatidylserine exposure and cell membrane
permeabilization). A selection of techniques that can be used to
distinguish apoptosis from necroptotic cells could be found in these
references.
Implication in disease
A section of mouse liver showing several apoptotic cells, indicated by arrowsA section of mouse liver stained to show cells undergoing apoptosis (orange)Neonatal cardiomyocytes ultrastructure after anoxia-reoxygenation
Defective pathways
The
many different types of apoptotic pathways contain a multitude of
different biochemical components, many of them not yet understood.
As a pathway is more or less sequential in nature, removing or
modifying one component leads to an effect in another. In a living
organism, this can have disastrous effects, often in the form of disease
or disorder. A discussion of every disease caused by modification of
the various apoptotic pathways would be impractical, but the concept
overlying each one is the same: The normal functioning of the pathway
has been disrupted in such a way as to impair the ability of the cell to
undergo normal apoptosis. This results in a cell that lives past its
"use-by date" and is able to replicate and pass on any faulty machinery
to its progeny, increasing the likelihood of the cell's becoming
cancerous or diseased.
A recently described example of this concept in action can be seen in the development of a lung cancer called NCI-H460. The X-linked inhibitor of apoptosis protein (XIAP) is overexpressed in cells of the H460 cell line. XIAPs bind to the processed form of caspase-9 and suppress the activity of apoptotic activator cytochrome c,
therefore overexpression leads to a decrease in the number of
proapoptotic agonists. As a consequence, the balance of anti-apoptotic
and proapoptotic effectors is upset in favour of the former, and the
damaged cells continue to replicate despite being directed to die.
Defects in regulation of apoptosis in cancer cells occur often at the
level of control of transcription factors. As a particular example,
defects in molecules that control transcription factor NF-κB in cancer
change the mode of transcriptional regulation and the response to
apoptotic signals, to curtail dependence on the tissue that the cell
belongs. This degree of independence from external survival signals, can
enable cancer metastasis.
Dysregulation of p53
The tumor-suppressor protein p53 accumulates when DNA is damaged due to a chain of biochemical factors. Part of this pathway includes alpha-interferon and beta-interferon, which induce transcription of the p53 gene, resulting in the increase of p53 protein level and enhancement of cancer cell-apoptosis. p53 prevents the cell from replicating by stopping the cell cycle
at G1, or interphase, to give the cell time to repair; however, it will
induce apoptosis if damage is extensive and repair efforts fail. Any disruption to the regulation of the p53 or interferon genes will result in impaired apoptosis and the possible formation of tumors.
Inhibition
Inhibition
of apoptosis can result in a number of cancers, inflammatory diseases,
and viral infections. It was originally believed that the associated
accumulation of cells was due to an increase in cellular proliferation,
but it is now known that it is also due to a decrease in cell death. The
most common of these diseases is cancer, the disease of excessive
cellular proliferation, which is often characterized by an
overexpression of IAP
family members. As a result, the malignant cells experience an abnormal
response to apoptosis induction: Cycle-regulating genes (such as p53,
ras or c-myc) are mutated or inactivated in diseased cells, and further
genes (such as bcl-2) also modify their expression in tumors. Some
apoptotic factors are vital during mitochondrial respiration e.g.
cytochrome C.
Pathological inactivation of apoptosis in cancer cells is correlated
with frequent respiratory metabolic shifts toward glycolysis (an
observation known as the "Warburg hypothesis".
HeLa cell
Apoptosis in HeLa
cells is inhibited by proteins produced by the cell; these inhibitory
proteins target retinoblastoma tumor-suppressing proteins. These tumor-suppressing proteins regulate the cell cycle, but are rendered inactive when bound to an inhibitory protein.
HPV E6 and E7 are inhibitory proteins expressed by the human
papillomavirus, HPV being responsible for the formation of the cervical
tumor from which HeLa cells are derived. HPV E6 causes p53, which regulates the cell cycle, to become inactive. HPV E7 binds to retinoblastoma tumor suppressing proteins and limits its ability to control cell division.hese two inhibitory proteins are partially responsible for HeLa cells' immortality by inhibiting apoptosis to occur.
Treatments
Further information on a clinical pathology test that measures apoptosis: MiCK assay
The main method of treatment for potential death from
signaling-related diseases involves either increasing or decreasing the
susceptibility of apoptosis in diseased cells, depending on whether the
disease is caused by either the inhibition of or excess apoptosis. For
instance, treatments aim to restore apoptosis to treat diseases with
deficient cell death and to increase the apoptotic threshold to treat
diseases involved with excessive cell death. To stimulate apoptosis, one
can increase the number of death receptor ligands (such as TNF or
TRAIL), antagonize the anti-apoptotic Bcl-2 pathway, or introduce Smac
mimetics to inhibit the inhibitor (IAPs).
The addition of agents such as Herceptin, Iressa, or Gleevec works to
stop cells from cycling and causes apoptosis activation by blocking
growth and survival signaling further upstream. Finally, adding p53-MDM2
complexes displaces p53 and activates the p53 pathway, leading to cell
cycle arrest and apoptosis. Many different methods can be used either to
stimulate or to inhibit apoptosis in various places along the death
signaling pathway.
Apoptosis is a multi-step, multi-pathway cell-death programme
that is inherent in every cell of the body. In cancer, the apoptosis
cell-division ratio is altered. Cancer treatment by chemotherapy and
irradiation kills target cells primarily by inducing apoptosis.
Hyperactive apoptosis
On
the other hand, loss of control of cell death (resulting in excess
apoptosis) can lead to neurodegenerative diseases, hematologic diseases,
and tissue damage. Neurons that rely on mitochondrial respiration
undergo apoptosis in neurodegenerative diseases such as Alzheimer's and Parkinson's. (an observation known as the "Inverse Warburg hypothesis"). Moreover, there is an inverse epidemiological comorbidity between neurodegenerative diseases and cancer.
The progression of HIV is directly linked to excess, unregulated
apoptosis. In a healthy individual, the number of CD4+ lymphocytes is
in balance with the cells generated by the bone marrow; however, in
HIV-positive patients, this balance is lost due to an inability of the
bone marrow to regenerate CD4+ cells. In the case of HIV, CD4+
lymphocytes die at an accelerated rate through uncontrolled apoptosis,
when stimulated.
At the molecular level, hyperactive apoptosis can be caused by defects
in signaling pathways that regulate the Bcl-2 family proteins. Increased
expression of apoptotic proteins such as BIM, or their decreased
proteolysis, leads to cell death and can cause a number of pathologies,
depending on the cells where excessive activity of BIM occurs. Cancer
cells can escape apoptosis through mechanisms that suppress BIM
expression or by increased proteolysis of BIM.
Treatments
Treatments
aiming to inhibit works to block specific caspases. Finally, the Akt
protein kinase promotes cell survival through two pathways. Akt
phosphorylates and inhibits Bad (a Bcl-2 family member), causing Bad to
interact with the 14-3-3
scaffold, resulting in Bcl dissociation and thus cell survival. Akt
also activates IKKα, which leads to NF-κB activation and cell survival.
Active NF-κB induces the expression of anti-apoptotic genes such as
Bcl-2, resulting in inhibition of apoptosis. NF-κB has been found to
play both an antiapoptotic role and a proapoptotic role depending on the
stimuli utilized and the cell type.
HIV progression
The progression of the human immunodeficiency virus infection into AIDS is due primarily to the depletion of CD4+ T-helper lymphocytes
in a manner that is too rapid for the body's bone marrow to replenish
the cells, leading to a compromised immune system. One of the mechanisms
by which T-helper cells are depleted is apoptosis, which results from a
series of biochemical pathways:
HIV enzymes deactivate anti-apoptotic Bcl-2. This does
not directly cause cell death but primes the cell for apoptosis should
the appropriate signal be received. In parallel, these enzymes activate
proapoptotic procaspase-8, which does directly activate the mitochondrial events of apoptosis.
HIV may increase the level of cellular proteins that prompt Fas-mediated apoptosis.
HIV proteins decrease the amount of CD4 glycoprotein marker present on the cell membrane.
Released viral particles and proteins present in extracellular fluid
are able to induce apoptosis in nearby "bystander" T helper cells.
HIV decreases the production of molecules involved in marking the
cell for apoptosis, giving the virus time to replicate and continue
releasing apoptotic agents and virions into the surrounding tissue.
The infected CD4+ cell may also receive the death signal from a cytotoxic T cell.
Cells may also die as direct consequences of viral infections. HIV-1 expression induces tubular cell G2/M arrest and apoptosis.
The progression from HIV to AIDS is not immediate or even necessarily
rapid; HIV's cytotoxic activity toward CD4+ lymphocytes is classified as
AIDS once a given patient's CD4+ cell count falls below 200.
Researchers from Kumamoto University in Japan have developed a
new method to eradicate HIV in viral reservoir cells, named "Lock-in and
apoptosis." Using the synthesized compound Heptanoylphosphatidyl
L-Inositol Pentakisphophate (or L-Hippo) to bind strongly to the HIV
protein PR55Gag, they were able to suppress viral budding. By
suppressing viral budding, the researchers were able to trap the HIV
virus in the cell and allow for the cell to undergo apoptosis (natural
cell death). Associate Professor Mikako Fujita has stated that the
approach is not yet available to HIV patients because the research team
has to conduct further research on combining the drug therapy that
currently exists with this "Lock-in and apoptosis" approach to lead to
complete recovery from HIV.
Viral infection
Viral induction of apoptosis occurs when one or several cells of a living organism are infected with a virus, leading to cell death. Cell death in organisms is necessary for the normal development of cells and the cell cycle maturation. It is also important in maintaining the regular functions and activities of cells.
Viruses can trigger apoptosis of infected cells via a range of mechanisms including:
Expression of viral proteins coupled to MHC proteins on the surface
of the infected cell, allowing recognition by cells of the immune system
(such as natural killer and cytotoxic T cells) that then induce the infected cell to undergo apoptosis.
Canine distemper virus (CDV) is known to cause apoptosis in central nervous system and lymphoid tissue of infected dogs in vivo and in vitro.
Apoptosis caused by CDV is typically induced via the extrinsic pathway, which activates caspases that disrupt cellular function and eventually leads to the cells death.
In normal cells, CDV activates caspase-8 first, which works as the
initiator protein followed by the executioner protein caspase-3.
However, apoptosis induced by CDV in HeLa cells does not involve the
initiator protein caspase-8. HeLa cell apoptosis caused by CDV follows a
different mechanism than that in vero cell lines. This change in the caspase cascade suggests CDV induces apoptosis via the intrinsic pathway,
excluding the need for the initiator caspase-8. The executioner protein
is instead activated by the internal stimuli caused by viral infection
not a caspase cascade.
The Oropouche virus (OROV) is found in the family Bunyaviridae. The study of apoptosis brought on by Bunyaviridae was initiated in 1996, when it was observed that apoptosis was induced by the La Crosse virus into the kidney cells of baby hamsters and into the brains of baby mice.
OROV is a disease that is transmitted between humans by the biting midge (Culicoides paraensis). It is referred to as a zoonoticarbovirus and causes febrile illness, characterized by the onset of a sudden fever known as Oropouche fever.
The Oropouche virus also causes disruption in cultured cells –
cells that are cultivated in distinct and specific conditions. An
example of this can be seen in HeLa cells, whereby the cells begin to degenerate shortly after they are infected.
With the use of gel electrophoresis, it can be observed that OROV causes DNA
fragmentation in HeLa cells. It can be interpreted by counting,
measuring, and analyzing the cells of the Sub/G1 cell population. When HeLA cells are infected with OROV, the cytochrome C
is released from the membrane of the mitochondria, into the cytosol of
the cells. This type of interaction shows that apoptosis is activated
via an intrinsic pathway.
In order for apoptosis to occur within OROV, viral uncoating,
viral internalization, along with the replication of cells is necessary.
Apoptosis in some viruses is activated by extracellular stimuli.
However, studies have demonstrated that the OROV infection causes
apoptosis to be activated through intracellular stimuli and involves the
mitochondria.
Many viruses encode proteins that can inhibit apoptosis.
Several viruses encode viral homologs of Bcl-2. These homologs can
inhibit proapoptotic proteins such as BAX and BAK, which are essential
for the activation of apoptosis. Examples of viral Bcl-2 proteins
include the Epstein-Barr virus BHRF1 protein and the adenovirus E1B 19K protein.
Some viruses express caspase inhibitors that inhibit caspase activity
and an example is the CrmA protein of cowpox viruses. Whilst a number of
viruses can block the effects of TNF and Fas. For example, the M-T2
protein of myxoma viruses can bind TNF preventing it from binding the
TNF receptor and inducing a response.
Furthermore, many viruses express p53 inhibitors that can bind p53 and
inhibit its transcriptional transactivation activity. As a consequence,
p53 cannot induce apoptosis, since it cannot induce the expression of
proapoptotic proteins. The adenovirus E1B-55K protein and the hepatitis B virus HBx protein are examples of viral proteins that can perform such a function.
Viruses can remain intact from apoptosis in particular in the latter stages of infection. They can be exported in the apoptotic bodies
that pinch off from the surface of the dying cell, and the fact that
they are engulfed by phagocytes prevents the initiation of a host
response. This favours the spread of the virus. Prions can cause apoptosis in neurons.
Plants
Programmed cell death
in plants has a number of molecular similarities to that of animal
apoptosis, but it also has differences, notable ones being the presence
of a cell wall and the lack of an immune system
that removes the pieces of the dead cell. Instead of an immune
response, the dying cell synthesizes substances to break itself down and
places them in a vacuole
that ruptures as the cell dies. Additionally, plants do not contain
phagocytic cells, which are essential in the process of breaking down
and removing apoptotic bodies. Whether this whole process resembles animal apoptosis closely enough to warrant using the name apoptosis (as opposed to the more general programmed cell death) is unclear.
Caspase-independent apoptosis
The
characterization of the caspases allowed the development of caspase
inhibitors, which can be used to determine whether a cellular process
involves active caspases. Using these inhibitors it was discovered that
cells can die while displaying a morphology similar to apoptosis without
caspase activation. Later studies linked this phenomenon to the release of AIF (apoptosis-inducing factor) from the mitochondria and its translocation into the nucleus mediated by its NLS (nuclear localization signal).
Inside the mitochondria, AIF is anchored to the inner membrane. In
order to be released, the protein is cleaved by a calcium-dependent calpain protease.
Palm oil block showing the lighter color that results from boiling
Palm oil is an edible vegetable oil derived from the mesocarp (reddish pulp) of the fruit of oil palms. The oil is used in food manufacturing, in beauty products, and as biofuel. Palm oil accounted for about 36% of global oils produced from oil crops in 2014. Palm oils are easier to stabilize and maintain quality of flavor and consistency in ultra-processed foods, so they are frequently favored by food manufacturers. Globally, humans consumed an average of 7.7 kg (17 lb) of palm oil per person in 2015.
Demand has also increased for other uses, such as cosmetics and
biofuels, encouraging the growth of palm oil plantations in tropical
countries.
The use of palm oil has attracted the concern of environmental and human right groups. The palm oil industry is a significant contributor to deforestation in the tropics
where palms are grown and has been cited as a factor in social problems
due to allegations of human rights violations among growers. The Roundtable on Sustainable Palm Oil
was formed in 2004 to promote the more sustainable and ethical
production of palm oil. However, very little palm oil is certified
through the organization, and some groups have criticized it as greenwashing.
In 2018, a report by the International Union for Conservation of Nature
acknowledged that palm oil is much more efficient than other oils in
terms of land and water usage; however, deforestation causes more
biodiversity loss than switching to other oils. The biggest global producers of palm oil are Indonesia, who produced 60% of it in 2022, followed by Malaysia, Thailand, and Nigeria. Indonesia produces biodiesel primarily from palm oil.
Humans used oil palms as far back as 5,000 years. In the late 1800s,
archaeologists discovered a substance that they concluded was originally
palm oil in a tomb at Abydos dating back to 3,000 BCE.
Palm oil from Elaeis guineensis has long been recognized in West and Central African countries, used widely as a cooking oil. European merchants trading with West Africa occasionally purchased palm oil for use as a cooking oil in Europe.
By around 1870, palm oil constituted the primary export of some
West African countries, which often led to oppressive labor practices,
as highlighted in the account of Abina Mansah's life. However, this was overtaken by cocoa in the 1880s with the introduction of colonial European cocoa plantations.
Processing
Oil palm fruits on the treeAn oil palm stem, weighing about 10 kg (22 lb), with some of its fruits picked
Palm oil is naturally reddish in color because of a high beta-carotene content. It is not to be confused with palm kernel oil derived from the kernel of the same fruit or coconut oil derived from the kernel of the coconut palm (Cocos nucifera). The differences are in color (raw palm kernel oil lacks carotenoids and is not red), and in saturated fat
content: palm mesocarp oil is 49% saturated, while palm kernel oil and
coconut oil are 81% and 86% saturated fats, respectively. However, crude
red palm oil that has been refined, neutralized, bleached and
deodorized, a common commodity called RBD (refined, bleached, and deodorized) palm oil, does not contain carotenoids.
Many industrial food applications of palm oil use fractionated
components of palm oil (often listed as "modified palm oil") whose
saturation levels can reach 90%; these "modified" palm oils can become highly saturated, but are not necessarily hydrogenated.
The oil palm produces bunches containing many fruits with the
fleshy mesocarp enclosing a kernel that is covered by a very hard shell.
The FAO
considers palm oil (coming from the pulp) and palm kernels to be
primary products. The oil extraction rate from a bunch varies from 17 to
27% for palm oil, and from 4 to 10% for palm kernels.
Along with coconut oil, palm oil is one of the few highly saturated vegetable fats and is semisolid at room temperature.
Palm oil is a common cooking ingredient in the tropical belt of Africa,
Southeast Asia and parts of Brazil. Its use in the commercial food
industry in other parts of the world is widespread because of its lower
cost and the high oxidative stability (saturation) of the refined product when used for frying. One source reported that humans consumed an average 17 pounds (7.7 kg) of palm oil per person in 2015.
Extraction
Red
Palm oil being sold on the side of the road in plastic bottles in
Ghana. Artisanal production of palm oil is common in Ghana, providing a
key staple food stuff in most traditional cooking.
Palm oil is traditionally, and still industrially, produced by milling the fruits of oil palm.
Besides milling, palm oil is produced by cold-pressing
the fruit of the oil palm since the 1990s. This type of artisanal palm
oil is usually not further refined, so they keep the natural red color.
It is bottled for use as a cooking oil, in addition to other uses such as being blended into mayonnaise and vegetable oil.
The result of milling or cold-pressing is a mixture of water,
crude palm oil, and fibers from the palm fruit. A minimum degree of
processing is required to obtain the oil. The mixture is first passed
through a filter to remove the solids, then separated by density to
removed the water. Density treatment can also act as a basic form of
degumming, provided that the fruit is steamed before milling to
hydrolyze the gum, at a cost of also losing some triglycerides to
hydrolysis.
The result of basic processing is called a "crude palm oil" or a "red palm oil", referring to its intense color due to the high caretinoid content. Red palm oil is a traditional cooking oil in West Africa. The free fatty acids within provide a "bite" to the flavor. The triglyceride part is around 50% saturated fat—considerably less than palm kernel oil—and 40% monounsaturated fat and 10% polyunsaturated fat. It is a source of Vitamin A and Vitamin E.
Worker
walking near the boundary of an oil mill in Malaysia. Palm oil
production is important part of economies in many parts of rural
Malaysia, but is also a source of environmental conflict
Crude PO can be refined to remove its non-triglyceride components.
Bleaching removes color from the oil. This is achieved by adding a clay absorbent called bleaching earth in a vacuum mixer.
Filters remove the clay from the oil.
The oil enters the deodorizer, which is responsible for removing free fatty acids
(FFA) generated by hydrolysis. One type of deodorizer works by
distillating out the FFAs using a set of different temperatures. The FFA
is collected as "palm fatty acid distillate" (PFAD). PFAD is itself a valuable product used in the manufacture of soaps, washing powder and other products.
The final, refined oil is called "refined, bleached and deodorized
palm oil" (RBD PO). RBD PO is the basic palm oil sold on the world's
commodity markets.
RBD PO is also known as white palm oil. It can be further fractionated
using the different melting points of its components. The part with a
higher melting point, which crystalizes out as a solid earlier, is
called palm stearin. It consists of mostly saturated fats. The remaining liquid part is called palm olein. It is also possible to fractionate at a different point of processing, even with crude palm oil.
RBD PO, or "palm shortening",
is extensively used in food manufacture. It is valued for its low
polyunsaturated fat content, which offers high stability against rancidity and allows it to replace hydrogenated fats in a variety of baked and fried products.
Uses
Palm
oil production is done in some parts of the world artisanally, and the
locally produced oil is used for food, handicrafts and other products.
This woman in the Democratic Republic of the Congo is showing the palm
fruit above a pot for processing the fruit.
In food
The highly saturated nature of palm oil renders it solid at room temperature in temperate regions, making it a cheap substitute for butter or hydrogenatedvegetable oils in uses where solid fat is desirable, such as the making of pastry dough and baked goods. Palm oil is used in West African cuisine such as egusi soup and okra soup. Palm oil is sometimes used as a minor ingredient in calf milk replacer.
Non-food consumer products
Palm
oil is pervasively used in personal care and cleaning products, and it
provides the foaming agent in nearly every soap, shampoo, or detergent.
Around 70% of personal care products including soap, shampoo, makeup,
and lotion, contain ingredients derived from palm oil. However, there
are more than 200 different names for these palm oil ingredients and
only 10% of them include the word "palm".
Biomass and biofuels
Palm oil is used to produce both methyl ester and hydrodeoxygenated biodiesel. Palm oil methyl ester is created through a process called transesterification. Palm oil biodiesel is often blended with other fuels to create palm oil biodiesel blends. Palm oil biodiesel meets the European EN 14214 standard for biodiesels. Hydrodeoxygenated biodiesel is produced by direct hydrogenolysis of the fat into alkanes and propane. The world's largest palm oil biodiesel plant is the €550 million Finnish-operated Neste Oil biodiesel plant in Singapore, which opened in 2011 with a capacity of 800,000 tons per year and produces hydrodeoxygenated NEXBTL biodiesel from palm oil imported from Malaysia and Indonesia.
Significant amounts of palm oil exports to Europe are converted to biodiesel (as of early 2018: Indonesia: 40%, Malaysia 30%).In 2014, almost half of all the palm oil in Europe was burned as car and truck fuel. As of 2018, one-half of Europe's palm oil imports were used for biodiesel. Use of palm oil as biodiesel generates three times the carbon emissions as using fossil fuel, and, for example, "biodiesel made from Indonesian palm oil makes the global carbon problem worse, not better."
There are pressures for increased oil palm production from
Indonesian palm-based biodiesel programs. The biodiesel currently
contains a 30:70 palm oil to conventional diesel ratio (known as B30) at
the gas pumps. The Indonesian government is aiming to produce 100% palm
oil biodiesel (or B100) to transition out of using conventional diesel.
The Indonesian government has estimated it would need to establish
approximately 15 million hectares of oil palm plantations to meet these
future demands.
The organic waste matter that is produced when processing oil
palm, including oil palm shells and oil palm fruit bunches, can also be
used to produce energy. This waste material can be converted into
pellets that can be used as a biofuel.
Additionally, palm oil that has been used to fry foods can be converted
into methyl esters for biodiesel. The used cooking oil is chemically
treated to create a biodiesel similar to petroleum diesel.
In wound care
Although palm oil is applied to wounds for its supposed antimicrobial effects, research does not confirm its effectiveness.
Production
In 2022–2023, world production of palm oil was 78 million metric tons (86 million short tons). The annual production of palm oil is projected to reach 240 million metric tons (260 million short tons) by 2050. During the 2022 food crises instigated by the Russian invasion of Ukraine and crop failures in other parts of the world due to extreme weather caused by climate change, the Indonesian government banned exports of palm oil.
This combined with a reduced harvest in Malaysia greatly increased
global prices, while reducing availability causing ripple effects in the
global supply chain. On 23 May 2022, the Indonesian government reopened trading hoping to balance supplies.
Indonesia
is the world's largest producer of palm oil, surpassing Malaysia in
2006, producing more than 20.9 million metric tons (23.0 million short
tons), a number that has since risen to over 34.5 million metric tons (38.0 million short tons) (2016 output). Indonesia expects to double production by the end of 2030. By 2019, this number was 51.8 million metric tons (57.1 million short tons). At the end of 2010, 60% of the output was exported in the form of crude palm oil. FAO data shows production increased by over 400% between 1994 and 2004, to over 8.7 million metric tons (9.6 million short tons).
A palm oil mill located on a palm oil plantation in MalaysiaA satellite image showing deforestation in Malaysian Borneo to allow the plantation of oil palm
In 2012, the country
produced 18.8 million metric tons (20.7 million short tons) of crude
palm oil on roughly 5,000,000 hectares (19,000 sq mi) of land.
Though Indonesia produces more palm oil, Malaysia is the world's
largest exporter of palm oil having exported 18 million metric tons
(20 million short tons) of palm oil products in 2011. India, China, Pakistan, the European Union and the United States are the primary importers of Malaysian palm oil products. In 2016, palm oil prices jumped to a four-year high days after Trump's election victory in the US.
Nigeria
As of 2018, Nigeria
was the third-largest producer, with approximately 2.3 million hectares
(5.7 million acres) under cultivation. Both small- and large-scale
producers participate in the industry. In much of the Niger Delta, palm oil is commonoly referred to as "red oil" (or red gold) to distinguish it from the "black oil" (crude oil) which dominates production.
Thailand
Thailand
is the world's third largest producer of crude palm oil, producing
approximately 2 million metric tons (2.2 million short tons) per year,
or 1.2% of global output. Nearly all of Thai production is consumed
locally. Almost 85% of palm plantations and extraction mills are in
south Thailand. At year-end 2016, 4.7 to 5.8 million rai
(750,000 to 930,000 hectares; 1,900,000 to 2,300,000 acres) were
planted in oil palms, employing 300,000 farmers, mostly on small
landholdings of 20 rai (3.2 hectares; 7.9 acres). ASEAN
as a region accounts for 52.5 million metric tons (57.9 million short
tons) of palm oil production, about 85% of the world total and more than
90% of global exports. Indonesia accounts for 52% of world exports.
Malaysian exports total 38%. The biggest consumers of palm oil are
India, the European Union, and China, with the three consuming nearly
50% of world exports. Thailand's Department of Internal Trade (DIT)
usually sets the price of crude palm oil and refined palm oil Thai
farmers have a relatively low yield compared to those in Malaysia and
Indonesia. Thai palm oil crops yield 4–17% oil compared to around 20% in
competing countries. In addition, Indonesian and Malaysian oil palm
plantations are 10 times the size of Thai plantations.
Benin
Palm is native to the wetlands of western Africa, and south Benin
already hosts many palm plantations. Its 'Agricultural Revival
Programme' has identified many thousands of hectares of land as suitable
for new oil palm export plantations. In spite of the economic benefits,
Non-governmental organisations (NGOs), such as Nature Tropicale, claim biofuels will compete with domestic food production in some existing prime agricultural sites. Other areas comprise peat land, whose drainage would have a deleterious environmental impact. They are also concerned genetically modified plants will be introduced into the region, jeopardizing the current premium paid for their non-GM crops.
According to recent article by National Geographic, most palm oil in Benin is still produced by women for domestic use. The FAO additionally states that peasants in Benin practice agroecology. They harvest palm fruit from small farms and the palm oil is mostly used for local consumption.
Cameroon
Cameroon had a production project underway initiated by Herakles Farms in the US.
However, the project was halted under the pressure of civil society
organizations in Cameroon. Before the project was halted, Herakles left
the Roundtable on Sustainable Palm Oil early in negotiations.
The project has been controversial due to opposition from villagers and
the location of the project in a sensitive region for biodiversity.
Colombia
In 2018, total palm oil production in Colombia reached 1.6 million metric tons (1.8 million short tons), representing some 8% of national agricultural GDP and benefiting mainly smallholders (65% of Colombia's palm oil sector).
According to a study from the Environmental, Science and Policy,
Colombia has the potential to produce sustainable palm oil without
causing deforestation. In addition, palm oil and other crops provide a productive alternative for illegal crops, like coca.
Ecuador
Ecuador
aims to help palm oil producers switch to sustainable methods and
achieve RSPO certification under initiatives to develop greener
industries.
Ghana
Ghana has a lot of palm nut
species, which may become an important contributor to the agriculture
of the region. Although Ghana has multiple palm species, ranging from
local palm nuts to other species locally called agric, it was only
marketed locally and to neighboring countries. Production is now
expanding as major investment funds are purchasing plantations, because
Ghana is considered a major growth area for palm oil.
Kenya
Kenya's
domestic production of edible oils covers about a third of its annual
demand, estimated at 380,000 metric tons (420,000 short tons). The rest
is imported at a cost of around US$140 million a year, making edible oil
the country's second most important import after petroleum. Since 1993 a
new hybrid variety of cold-tolerant, high-yielding oil palm has been promoted by the Food and Agriculture Organization of the United Nations
in western Kenya. As well as alleviating the country's deficit of
edible oils while providing an important cash crop, it is claimed to
have environmental benefits in the region, because it does not compete
against food crops or native vegetation and it provides stabilisation
for the soil.
Myanmar
Palm oil was introduced to British Burma (now Myanmar) in the 1920s. Beginning in the 1970s, smaller-scale palm oil plantations were developed in Tanintharyi Region, and Mon, Kayin, and Rakhine States. In 1999, the ruling military junta, the State Peace and Development Council, initiated the large-scale development of such plantations, especially in Tanintharyi, the southernmost region of Myanmar. As of 2019, over 401,814 ha of palm oil concessions have been awarded to 44 companies.
60% of the awarded concessions consist of forests and native
vegetation, and some concessions overlap with national parks, including Tanintharyi and Lenya National Parks, which have seen deforestation and threaten conservation efforts for endemic species like the Indochinese tiger.
In Borneo, the forest (F), is being replaced by oil palm plantations (G). These changes are irreversible for all practical purposes (H).
In addition to environmental concerns, palm oil development in regions that produce it has also led to significant social conflict.
Regions with fast growing palm oil production have experienced
significant violations of indigenous land rights, influxes of illegal
immigrant labor and labor practices, and other alleged related human
rights violations.
The palm oil industry has had both positive and negative impacts on workers, indigenous peoples
and residents of palm oil-producing communities. Palm oil production
provides employment opportunities, and has been shown to improve infrastructure, social services and reduce poverty.
However, in some cases, oil palm plantations have developed lands
without consultation or compensation of the indigenous people inhabiting
the land, resulting in social conflict. The use of illegal immigrants in Malaysia has also raised concerns about working conditions within the palm oil industry.
Some social initiatives use palm oil cultivation as part of
poverty alleviation strategies. Examples include the UN Food and
Agriculture Organisation's hybrid oil palm project in Western Kenya,
which improves incomes and diets of local populations, and Malaysia's Federal Land Development Authority and Federal Land Consolidation and Rehabilitation Authority, which both support rural development.
The use of palm oil in the production of biodiesel has led to
concerns that the need for fuel is being placed ahead of the need for
food, leading to malnutrition in developing nations. This is known as the food versus fuel debate. According to a 2008 report published in the Renewable and Sustainable Energy Reviews,
palm oil was determined to be a sustainable source of both food and
biofuel, and the production of palm oil biodiesel does not pose a threat
to edible palm oil supplies. According to a 2009 study published in the Environmental Science and Policy
journal, palm oil biodiesel might increase the demand for palm oil in
the future, resulting in the expansion of palm oil production, and
therefore an increased supply of food.
Human rights
The
Palm oil industry has a history of violating labor-related human
rights, indigenous territorial right and environmental rights of
communities in the contexts where the industry is prominent. Child labor
violations are common in smallholder farming in many of the
post-colonial contexts (such as Africa) in which palm oil is produced.
One report indicated numerous allegations of human rights violations in the production of palm oil in Indonesia and Malaysia, including exposure to hazardous pesticides, child labor, and rape and sexual abuse,
and unsafe carrying loads. These incidents may receive no response by
the company or police, or are left unreported because victims fear
retaliation from their abuser. The chemicals used in the pesticides,
such as paraquat and glyphosate, have been linked to diseases such as Parkinson's disease and cancer.
Reports of Indigenous peoples and communities in Indonesia,
indicate losing farmland and traditionally significant land due to palm
oil industry expansion. In 2017, there were over 650 different land
disputes between palm oil plantations and Indigenous land owners. Indigenous communities also expressed concern over the loss of natural resources, such as wild rubber, reed, and adat forests (communal forests). Indigenous communities have made some ground when it comes to land disputes, either through protest or legal means.
Other concerns when it comes to Indigenous communities being
impacted include lack of government oversight on palm oil plantations,
political corruption, or the lacking of enforcement on laws meant to
protect Indigenous lands.
In countries such as Guatemala, palm oil plantations have significant
leverage within the local justice system, leading local police to
disregard land claims, going as far as using force to break up protests,
and even murdering local leaders.
While only 5% of the world's vegetable oil farmland is used for palm
plantations, palm cultivation produces 38% of the world's total
vegetable oil supply. In terms of oil yield, a palm plantation is 10 times more productive than soybean, sunflower or rapeseed cultivation because the palm fruit and kernel both provide usable oil.
Palm oil has garnered criticism from environmentalists due to the
environmental importance of where it is grown. However, it is
indisputably more efficient in comparison to other oil-producing plants.
In 2016, it was found that palm oil farms produce around 4.17 metric
tons of oil per hectare. By contrast other oils, such as sunflower,
soybean, or peanut only produce 0.56, 0.39, and 0.16 metric tons
respectively per hectare.
Palm oil is the most sustainable vegetable oil in terms of yield,
requiring one-ninth of land used by other vegetable oil crops. In the future, laboratory-grown microbes might achieve higher yields per unit of land at comparable prices.
However, palm oil cultivation has been criticized for its impact on the natural environment,including deforestation, loss of natural habitats, and greenhouse gas emissions which have threatened critically endangered species, such as the orangutan and Sumatran tiger. Slash-and-burn
techniques are still used to create new plantations across palm oil
producing countries. From January to September 2019, 857,000 hectares of
land was burned in Indonesia; peatlands accounted for more than a
quarter of the burned area.
The widespread deforestation and other environmental destruction in
Indonesia, much of which is caused by palm oil production has often been
described by academics as an ecocide.
Environmental groups such as Greenpeace and Friends of the Earth oppose the use of palm oil biofuels, claiming that the deforestation
caused by oil palm plantations is more damaging for the climate than
the benefits gained by switching to biofuel and using the palms as carbon sinks.
A 2018 study by the International Union for Conservation of Nature
(IUCN) concluded that palm oil is "here to stay" due to its higher
productivity compared with many other vegetable oils. The IUCN maintains
that replacing palm oil with other vegetable oils would necessitate
greater amounts of agricultural land, negatively affecting biodiversity.
The IUCN advocates better practices in the palm oil industry, including
the prevention of plantations from expanding into forested regions and
creating a demand for certified and sustainable palm oil products.
In 2019, the Rainforest Action Network surveyed eight global brands involved in palm oil extraction in the Leuser Ecosystem, and said that none was performing adequately in avoiding "conflict palm oil". Many of the companies told the Guardian they were working to improve their performance. A WWF scorecard rated only 15 out of 173 companies as performing well.
In 2020 a study by Chain Reaction Research
concluded that NDPE (No Deforestation, No Peat, No Exploitation)
policies cover 83% of palm oil refineries. NDPE policies are according
to the Chain Reaction Research the most effective private mechanism to
cut the direct link with deforestation, due to the economic leverage
refineries have over palm oil growers.
Markets
Palm oil is one of the most commonly produced vegetable oils
According to the Hamburg-based Oil World trade journal,
in 2008 global production of oils and fats stood at 160 million tonnes.
Palm oil and palm kernel oil were jointly the largest contributor,
accounting for 48 million tonnes, or 30% of the total output. Soybean oil
came in second with 37 million tonnes (23%). About 38% of the oils and
fats produced in the world were shipped across oceans. Of the 60 million
tonnes of oils and fats exported around the world, palm oil and palm
kernel oil made up close to 60%; Malaysia, with 45% of the market share,
dominated the palm oil trade. Production of palm oil that complies with
voluntary sustainability standards is growing at a faster rate than
conventional production. Standard-compliant production increased by 110%
from 2008 to 2016, while conventional production increased by 2%. The production of vegetable oils as a whole went up 125% between 2000 and 2020, driven by a sharp increase in palm oil.
Food label regulations
Previously,
palm oil could be listed as "vegetable fat" or "vegetable oil" on food
labels in the European Union (EU). From December 2014, food packaging
in the EU is no longer allowed to use the generic terms "vegetable fat"
or "vegetable oil" in the ingredients list. Food producers are required
to list the specific type of vegetable fat used, including palm oil.
Vegetable oils and fats can be grouped together in the ingredients list
under the term "vegetable oils" or "vegetable fats" but this must be
followed by the type of vegetable origin (e.g., palm, sunflower, or
rapeseed) and the phrase "in varying proportions".
In Malaysia, it is illegal to label products in ways that "discriminate against" palm oil. Offenders can be fined up to RM250,000 or imprisoned for up to five years.
Supply chain institutions
Consumer Goods Forum
In 2010, the Consumer Goods Forum
passed a resolution that its members would reduce deforestation to net
zero by 2020. They planned to do this through sustainable production of
several commodities, including palm oil. As of 2023 that goal has not been met.
Roundtable on Sustainable Palm Oil (RSPO)
Roundtable No 2 (RT2) in Zürich in 2005
The Roundtable on Sustainable Palm Oil (RSPO) was established in 2004 with the objective of promoting the growth and use of sustainable palm oil products through global standards and multistakeholder governance. The seat of the association is in Zürich, Switzerland, while the secretariat is currently based in Kuala Lumpur, with a satellite office in Jakarta. RSPO currently has 5,650 members from 94 countries.
The RSPO was established following concerns raised by
non-governmental organizations about environmental impacts resulting
from palm oil production.
51,999,404 metric tonnes of palm oil produced in 2016 was RSPO certified. Products containing Certified Sustainable Palm Oil (CSPO) can carry the RSPO trademark. Members of the RSPO include palm oil producers, environmental groups, and manufacturers who use palm oil in their products. In 2014, Indonesia accounted for 40% of global palm oil production and 44% of the total RSPO-certified areas.
After the meeting in 2009, a number of environmental organisations were critical of the scope of the agreements reached.
Palm oil growers who produce CSPO have been critical of the
organization because, though they have met RSPO standards and assumed
the costs associated with certification, the market demand for certified
palm oil remains low.
Even though deforestation has decreased in RSPO-certified oil palm
plantations, peatlands continue to be drained and burned for the
creation of new RSPO-certified palm plantations.
Left, reddish palm oil made from the pulp of oil palm fruit. Right, clear palm kernel oil made from the kernels
Nutrition, composition and health
Palm oil is a food staple in many cuisines, contributing significant calories as well as fat. Globally, humans consumed an average of 7.7 kg (17 lb) of palm oil per person in 2015. Although the relationship of palm oil consumption to disease risk has been previously assessed, the quality of the clinical research specifically assessing palm oil effects has been generally poor.
Consequently, research has focused on the deleterious effects of palm
oil and palmitic acid consumption as sources of saturated fat content in
edible oils, leading to conclusions that palm oil and saturated fats
should be replaced with polyunsaturated fats in the diet.
A 2015 meta-analysis and 2017 advisory from the American Heart Association indicated that palm oil is among foods supplying dietary saturated fat which increases blood levels of LDL cholesterol
and increased risk of cardiovascular diseases, leading to
recommendations for reduced use or elimination of dietary palm oil in
favor of consuming unhydrogenatedvegetable oils.
A 2019 meta-analysis found no association between total fat, saturated
fatty acids, monounsaturated fatty acid, and polyunsaturated fatty acid
intake with risk of cardiovascular disease.
Glycidyl fatty acid esters (GE), 3-MCPD
and 2-MCPD, are found especially in palm oils and palm fats because of
their refining at high temperatures (approx. 200 °C (392 °F)). Since glycidol, the parent compound of GE, is considered genotoxic and carcinogenic, the EFSA
did not set a safe level for GE. According to the chair of the CONTAM
(EFSA's expert Panel on Contaminants in the Food Chain), "The exposure
to GE of babies consuming solely infant formula is a particular concern as this is up to ten times what would be considered of low concern for public health". The EFSA's tolerable daily intake (TDI) of 3-MCPD
and its fatty acid esters was set to 0.8 micrograms per kilogram of
body weight per day (μg/kg bw/day) in 2016 and increased to 2 μg/kg
bw/day in 2017, based on evidence linking this substance to organ damage
in animal tests and on possible adverse effects on the kidney and on male fertility. According to the EFSA, there is not enough data to set a safe level for 2-MCPD. As of December 2022, the Malaysian Palm Oil Board
issued an amendment to its palm oil licensing conditions to include
maximum limits of 1.25 ppm and 1 ppm, respectively, to the amount of
3-MCPDE and GE that can be found in processed palm oil.
Palm oil, like all fats, is composed of fatty acids, esterified with glycerol. Palm oil has an especially high concentration of saturated fat, specifically the 16-carbon saturated fatty acid, palmitic acid, to which it gives its name. Monounsaturated oleic acid is also a major constituent of palm oil. Unrefined palm oil is a significant source of tocotrienol, part of the vitamin E family.
The linoleic acid content of palm oil is about 6,4 - 15%.
The approximate concentration of esterified fatty acids in palm oil is:
Fatty acid content of palm oil (present as triglyceride esters)
Red palm oil is rich in carotenes, such as alpha-carotene, beta-carotene and lycopene, which give it a characteristic dark red color.
However, palm oil that has been refined, bleached and deodorized from
crude palm oil (called "RBD palm oil") does not contain carotenes.
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