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Environment and Brain Student Presentations > Heavy Metals (Arsenic, Mercury, Cadmium, and Lead) > Flashcards

Heavy Metals (Arsenic, Mercury, Cadmium, and Lead) Flashcards

1
Q

Describe why lead may be an important environmental toxin. (2)

A
  • Found in Earth’s crust and easily mined and refined
  • Widespread use makes it one of the most pervasive environmental pollutants
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2
Q

Give seven environmental sources of lead (excluding occupational exposures). (7)

A
  • Paint (before 1978)
  • Ceramics
  • Plumbing (lead pipes; leaches into drinking water)
  • Leaded gasoline
  • Batteries
  • Cosmetics
  • Contaminated soil and dust
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3
Q

Give three occupational risks for lead exposure. (3)

A
  • Lead mining and refining
  • Smelting
  • Battery manufacturing and recycling
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4
Q

Give five dangers to humans of lead exposure. (5)

A
  • Neurotoxin that interferes with normal brain development
  • Impairments in cognition; learning; behaviour
  • Intellectual disability (lower IQ)
  • Cardiovascular disease
  • Kidney disease
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5
Q

Give three ways that humans can take in lead from the atmosphere. (3)

A
  • Inhalation of lead dust
  • Ingestion
  • Absorption through skin
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6
Q

Fill in the gaps relating to human exposure to lead. (3)

Lead gets stored in ………………….. and …………………., however human exposure is measured by …………………………

A

bones

teeth

blood lead (Pb) levels

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7
Q

Give nine acute symptoms of lead exposure in children. (9)

A
  • Joint and muscle pain
  • Headaches
  • Fatigue
  • Nausea
  • Loss of appetite
  • Weight loss
  • Seizures
  • Developmental delay
  • Irritability
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8
Q

Give six acute symptoms of lead exposure in adults. (6)

A
  • Joint and muscle pain
  • Headaches
  • Hypertension
  • Memory and concentration problems
  • Mood swings
  • Fertility issues (low sperm count; miscarriages; stillbirths)
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9
Q

Give five groups of people at high risk from lead exposure. (5)

A
  • Children (especially under 6yrs)
  • Pregnant women
  • Occupational groups
  • Low-income communities
  • People living in housing built before 1978
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10
Q

What historical event may be linked to lead exposure? (1)

Explain the reasons behind this. (2)

A

Decline of the roman empire

  • Lead was used in water pipes
  • Dining vessels/crockery also used lead (and wine acidity increases leaching)
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11
Q

A roman emperor who would have been exposed to more lead (perhaps from drinking more wine), showed what three symptoms? (3)

A
  • Mood swings
  • Epileptic seizures
  • Affected cognition
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12
Q

Give four general effects that lead has on the brain. (4)

A
  • Disruption of NT release (DA, 5HT, glutamate)
  • Structural changes in PFC; hippocampus; amygdala
  • Neuroinflammation, cytokines, and ROS
  • Disrupted neuroplasticity (altered formation/organisation of neuronal connections)
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13
Q

Describe the main mechanism by which lead can have an effect on the brain. (7)

A
  • Penetrates BBB (via passive diffusion; transporter-mediated uptake; disruption of integrity)
  • May imitate calcium ions (similar radius and charge)
  • Competes with calcium for transport across cell membranes
  • Disruption of calcium homeostasis and intracellular processes
  • BBB integrity is Ca-dependent (Pb interferes with and disrupts tight junctions; increasing permeability)
  • More neurotoxic substances enter brain
  • Also, activation of VGCCs and increased intracellular calcium
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14
Q

Briefly summarise the mechanism by which lead affects the brain. (1)

A

Imitates calcium

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15
Q

Describe how leaded petrol used to affect the environment and humans. (5)

A
  • Used commonly as thought to enhance engine performance
  • Combustion releases lead pollution into atmosphere
  • Increased emissions; contaminated air, dust, soil, drinking water, crops
  • Especially in urban areas and near motorways
  • Inhalation (esp, childhood and prenatal) leads to neurotoxicity and cognitive impairment
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16
Q

Describe how environmental and human effects from leaded petrol have been mitigated. (1)

What effect has this has on the environment and humans? (1)

A
  • Lead additives to petrol phased out between 1970 and 1990
  • Significant reduction in pollution levels and environmental exposure, and increased average IQ
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17
Q

Give three potential treatments for human lead exposure. (3)

A
  • Calcium or iron nutritional supplementation
  • GI decontamination
  • Chelation therapy
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18
Q

How does country development affect the risk from lead exposure? (1)

A

Underdeveloped countries at higher risk

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19
Q

Give three legislations in place aimed to mitigate the dangers of lead exposure. (3)

A
  • Workplace legislations (prevention and control exposure)
  • Drinking water quality legislations
  • EU ban leaded gasoline
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20
Q

Give three environmental sources of arsenic. (3)

A
  • Mine spills
  • Industrial waste
  • Chemicals used in agriculture
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21
Q

Describe how environmental sources of arsenic may make their way into humans. (3)

A
  • Groundwater contamination
  • Soil degradation and bioaccumulation
  • Human ingestion (via crops, drinking water etc)
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22
Q

Name a crop which is particularly good at storing arsenic. (1)

A

Rice

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23
Q

Give four reasons why arsenic may be particularly high in arsenic. (4)

A
  • Rice good at absorbing water and nutrients from soil
  • Rice paddies can be flooded for cultivation, leading to contamination
  • Arsenic-based pesticides can be used
  • Processing and cooking methods may not remove arsenic
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24
Q

Give four symptoms of arsenic poisoning. (4)

A
  • Skin pigmentation
  • Low blood pressure
  • Chest pains
  • Death
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25
Q

Give 11 dangers to human health of chronic, low doses of arsenic. (11)

A
  • Alzheimer’s disease
  • Cognitive deficits and diseases
  • Cancer
  • Skin lesions
  • CV diseases
  • Renal damage
  • Peripheral neuropathy
  • Encephalopathy
  • Liver damage
  • Diabetes
  • Bone marrow depression
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26
Q

True or false? Explain your answer if necessary. (1)

The dangers to human health of arsenic exposure are the same for adults as they are for children.

A

True - no age bias

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27
Q

Give three mechanisms of arsenic exposure in humans. (3)

A
  • Ingestion
  • Inhalation
  • Skin absorption
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28
Q

Once arsenic is in the body it accumulates in tissues and organs.

Give four places in particular where it accumulates. (4)

A
  • Skin
  • Lungs
  • Liver
  • Kidneys
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29
Q

Describe the excretion (method and amount) of arsenic once it is in the body. (2)

A

~70% excreted by kidneys

Rest may stay in body

30
Q

Describe how arsenic is converted to its ‘active’ metabolites in the body. (2)

A
  • Metabolic transformation in liver
  • To produce methylated metabolites (monomethylarsonic acid and dimethylarsonic acid)
31
Q

Can arsenic cross the blood brain barrier? (1)

A

Unknown - but its methylated metabolites do, via an unknown mechanism (perhaps passive diffusion or active transport)

32
Q

Give six mechanisms by which arsenic may cause damage to the brain. (6)

A
  • ROS production (via mitochondrial and ER dysfunction)
  • Damage to lipids, proteins, DNA
  • Activation of microglia and neuroinflammation
  • Neurotransmitter dysregulation (increased DA & 5HT, decreased NA)
  • Impaired synaptic transmission, learning, and memory
  • Interferes with glucocorticoid signalling, which affects 5HT in hippocampus
33
Q

Fill the gaps relating to arsenic exposure. (4)

Prenatal exposure has been linked to deficits in offspring ………………….., and childhood exposure is linked to lower ………………………..
……………………. is lowered by 5-10 points.

Long-term, chronic exposure is also linked to ………………………… in adults.

A

cognition

cognitive test scores

IQ

cognitive dysfunction

34
Q

Perinatal exposure to arsenic in mice has been linked with ……………………….. in the forced swim test. This indicates …………………………

A

increased immobility

depression

35
Q

Give three ways that arsenic exposure and its effects on the brain may contribute to Alzheimer’s disease. (3)

A
  • ROS
  • Neuroinflammation
  • Interference with APP
36
Q

Give five risk factors for increased effects of arsenic exposure. (5)

A
  • Genetic predisposition
  • Nutritional status
  • Co-exposure to other toxins
  • Duration and intensity of exposure
  • Geographical location
37
Q

Give three potential treatment options (with examples) for arsenic exposure. (3)

A
  • Antioxidants (vitamins C/E; selenium; alphalinoleic acid)
  • Chelation therapy (DMSA; DMPS)
  • Symptomatic treatment (antidepressants; cognitive enhancers)
38
Q

Give five mitigation/legislation strategies to help combat arsenic exposure. (5)

A
  • Improve water and soil management
  • Genetic modification of rice plants with aquaporin channels or CRISPR/Cas9 to prevent accumulation
  • Legislation on maximum arsenic levels varies globally
  • More funding for education in areas of higher risk
  • Climate change may increase uptake of arsenic by crops
39
Q

What is the physiological function of cadmium in humans? (1)

A

No physiological function

40
Q

Cadmium is used as a co-factor for which enzyme, in a species of marine diatom? (1)

A

Carbonic anhydrase

41
Q

Give three previous uses of cadmium. (3)

A
  • Paint pigment
  • Plating nonferrous alloys
  • Plastic stabiliser
42
Q

Give three current uses of cadmium. (3)

A
  • Ni-Cd batteries
  • Photovoltaic cells
  • Lab lasers
43
Q

Give three environmental sources of everyday cadmium exposure. (3)

A
  • Smoking (tobacco)
  • Food (contaminated soil; seafood; oilseeds)
  • Inhalation from atmosphere (metal refinery air pollution)
44
Q

Give four occupational sources of cadmium exposure. (4)

A
  • Electroplating
  • Battery manufacturing
  • Contaminant in zinc ores (mining)
  • Metal smelting
45
Q

Give two methods of cadmium intake in humans. (2)

Which leads to faster absorption? (1)

A
  • Respiratory (fastest absorption)
  • GI ingestion (slower absorption)
46
Q

Give three organs or tissues where cadmium is distributed to once in the body. (3)

A
  • Lungs
  • Liver
  • Kidneys
47
Q

Describe the discrepancy between cadmium absorption and excretion in the body. (1)

A

5% cadmium is absorbed but only 0.005% is excreted

48
Q

Give five symptoms of acute cadmium exposure. (5)

A
  • Giddiness
  • Vomiting
  • Syncope
  • Respiratory difficulty
  • Cramps
49
Q

Give five long-term dangers to human health from cadmium exposure. (5)

A
  • Cancer
  • Damage to brain, kidneys, and testes
  • Reproductive dysfunction
  • Osteomalacia
  • Oedema
50
Q

Name a specific medical condition caused by cadmium poisoning. (1)

Where in the world is it prevalent? (1)

What were the exact causes? (2)

A

Itai-Itai disease

Affected Japan

  • Mining pollution of rivers
  • Increased Cd levels in rice
51
Q

Describe the symptoms seen in Itai-Itai disease, and describe the general cause. (3)

A
  • Severe osteomalacia
  • Kidney failure

*Particularly seen in postmenopausal women

Due to cadmium poisoning

52
Q

True or false? Explain your answer if necessary. (1)

Itai-Itai disease is a historical disease, and has now been eradicated.

A

False - pollution protection agencies try to prevent similar outbreaks, however it has still been diagnosed in 2005

53
Q

Give eleven effects/mechanisms of cadmium on the brain. (11)

A
  • Disrupts NT production/release
  • Structural damage to membranes
  • Compromises cellular integrity
  • Oxidative stress
  • Lipid peroxidation; protein dysfunction; DNA damage
  • Disruption of calcium channels (altered calcium homeostasis; impaired synaptic transmission; neuronal excitability; NT release)
  • Triggers apoptotic pathways
  • Disrupted neuronal networks; neurodegeneration; neuroinflammation
  • Dendritic spine loss and neuronal shrinkage
  • Alterations in DA; 5HT; glutamate signalling
  • Alterations in cognitive and behavioural function
54
Q

Give three cognitive/behavioural changes seen with cadmium exposure. (3)

A
  • Impaired learning/memory
  • Decreased locomotor activity
  • Increased anxiety
55
Q

Give four general risk factors for increased effects of cadmium exposure. (4)

A
  • Genetic susceptibility
  • Age (young children and foetuses more vulnerable)
  • Exposure levels (including co-exposure to lead and mercury)
  • Lifestyle (smoking; alcohol; occupation)
56
Q

Give four genetic risk factors which may increase the effects of cadmium exposure. (4)

A
  • Mutations in genes related to oxidative stress response
  • Mutations in genes related to detoxification pathways
  • Mutations in genes related to neuronal function
  • Epigenetic modifications of genes involved in cadmium metabolism and neurotoxicity
57
Q

Give two potential treatment categories (with examples) for cadmium toxicity. (2)

Also give a potential future treatment. (1)

A
  • Antioxidants (gallic acid; ascorbic acid)
  • EDTA (chelating agent)

Future: arrestin domain-containing protein 1-mediated microvesicles (ARMMs)

58
Q

Give six mitigation/legislation strategies which aim to reduce cadmium poisoning. (6)

A
  • Screening and breeding rice which does not accumulate cadmium (CRISPR/Cas9)
  • Treating metal mining pollution in rivers (Water and Abandoned Metal Mines Programme (WAMM))
  • Restriction of hazardous substances in electrical and electronic equipment
  • Hazardous substances and packaging regulations
  • Ban of cadmium in cosmetic products
  • Water quality regulations
59
Q

Describe the current state of cadmium levels in foods in India and China, and also in Europe. (2)

A
  • Cd toxicity still high in certain foods (rice) in India and China
  • Europe shows increasing cadmium levels in soil
60
Q

Give six environmental sources of mercury. (6)

A
  • Batteries
  • Measuring devices (thermometers; barometers)
  • Lamps and light bulbs
  • Dental fillings (used to bind alloy particles together in silver fillings; can release low levels of vapours when put in or removed)
  • Some pharmaceuticals
  • Skin lightening products
61
Q

Give the three forms of mercury in the environment. (3)

A
  • Elemental (has not reacted with other compounds)
  • Inorganic (Combined with other elements not carbon; people may be exposed through occupation such as inhalation of vapours during industrial processes)
  • Organic (combined with carbon, eg. methylmercury)
62
Q

Which form of mercury is dangerous to humans? (1)

A

Methylmercury - it is highly toxic

63
Q

How is methylmercury formed? (1)

How are humans exposed to it? (1)

A

Formed when inorganic mercury circulating in general environment is dissolved in seawater or freshwater

Absorbed through diet (eg. shellfish, seafood)

64
Q

What was the Minamata Bay event in Japan? (2)

A

Acetic acid factory deposited waste containing methylmercury into Minamata Bay

Contaminated fish and shellfish which people went on to consume over long periods of time

65
Q

Give five symptoms of Minamata disease (or Russell-Hunter syndrome). (5)

What is the general cause of Minamata disease? (1)

A
  • Ataxia
  • Speech impairment
  • Peripheral neuropathy
  • Cerebral palsy
  • Cognitive decline

Caused by mercury toxicity

66
Q

Give nine risk factors for mercury toxicity. (9)

A
  • Dietary habits (selenium may mitigate mercury toxicity)
  • Smoking
  • Alcohol consumption
  • Occupational exposures
  • Heavy metals
  • Pesticides
  • Air pollution and industrial emissions
  • Developmental stage (worse during critical periods of brain development)
  • Pre-existing neurological conditions (Alzheimer’s/Parkinson’s)
67
Q

Describe five general mechanisms by which mercury can cause damage to the brain. (5)

A
  • Direct neurotoxicity (Penetrate BBB; accumulates in brain; disrupts neuronal structure and function)
  • Oxidative stress (generate ROS and impair antioxidant defence)
  • Neuroinflammation
  • Disruption of neurotransmission (interferes with glutamate, DA, ACh; disrupted synaptic signalling, impaired neuronal communication)
  • Amyloid beta and tau aggregation and accumulation
68
Q

Give three gene alterations which may interact with mercury toxicity and enhance effects. (3)

A
  • Polymorphisms in genes encoding glutathione-related enzymes which affect detoxification pathways (glutathione S-transferases; glutathione peroxidases)
  • SNPs affecting proteins involved in mercury metabolism; transport; and cellular response
  • Polymorphisms in regulatory regions of genes encoding mercury transporters; antioxidant enzymes; inflammatory mediators (altered gene expression)
69
Q

Give five treatments (with examples where appropriate) for mercury poisoning. (5)

A
  • Chelating agents (British anti-Lewisite good; DMSA & DMPS showed no effect)
  • Oxygen/Intubation
  • IV fluid replacement
  • Washing of skin with soap and water
  • GI decontamination with activated charcoal; whole-bowel irrigation with polyethene glycol
70
Q

Give four reasons why mercury is considered a chemical of global concern. (4)

A
  • Long-range atmospheric transport
  • Environmental persistence
  • Ability to bioaccumulate
  • Significant consequences on human health
71
Q

True or false? Explain your answer if necessary. (1)

There have been multiple legal cases providing compensation to Minamata Bay victims.

A

True

72
Q

Give a potential biomarker for mercury toxicity. (1)

A

Selenoprotein

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