Public Health 150 Environmental Health · st r a b ism u s Tw itc hi ng of the ex tr em ities and v...

Public Health 150 Environmental Health

John R. Froines, PhD Department of Environmental Health Sciences

Pesticides and Fumigants: Fate and Transport: Major CA controversy

Fumigant use in California

• Methyl iodide: Proposed use primarily for strawberries-methyl iodide to replace methyl bromide

• Chloropicrin

• Metam sodium

• Methyl bromide

• 1,3-dichloropropene (telone)

• Historically: DBCP and ethylene dibromide

Methods of Application

Shank injection application Bedded tarped application

Geographic Trends in Fumigant Use

0

10

20

30

40

50

19

88

19

89

19

90

19

91

19

92

19

93

19

94

19

95

19

96

19

97

19

98

19

99

20

00

20

01

20

02

20

03

20

04

20

05

20

06

20

07

20

08

20

09

20

10

Use of Soil Fumigants in California, 1988–2010

Metam Na&K

Methyl Bromide

Chloropicrin

1,3-Dichloropropene (Telone)

Mil

lio

ns

of

po

un

ds

of

acti

ve i

ngred

ien

t

P16 Criteria Crop Chloropicrin Metam Sodium Methyl Bromide 1,3-

Dichloropropene

Total

Pounds

Pounds PCT Pounds PCT Pounds PCT Pounds PCT

> 5

PC

T

Potatoes 200,000 < 1 31,700,000 20 200,000 <1 9,900,000 5 42,000,000

Tomatoes 1,700,000 10 7,000,000 15 10,600,00

0

20 300,000 < 1 19,600,000

Tobacco 3,600,000 15 100,000 < 1 500,000 < 1 7,800,000 10 12,000,000

Carrots 70,000 < 1 9,000,000 40 70,000 < 1 1,500,000 10 10,640,000

Strawberries 1,400,000 20 200,000 < 1 7,600,000 50 400,000 5 9,600,000

Peppers 700,000 10 700,000 5 3,700,000 20 200,000 5 5,300,000

Watermelons 800,000 < 1 700,000 2 2,300,000 5 400,000 < 1 4,200,000

Onions 200,000 < 1 1,700,000 5 200,000 < 1 900,000 5 3,000,000

Cucumbers 100,000 5 300,000 < 1 1,300,000 5 900,000 10 2,600,000

Peanuts 5,000 < 1 1,100,000 5 1,300,000 < 1 2,405,000

Cantaloupes 100,000 5 800,000 5 800,000 5 300,000 5 2,000,000

Sweet Potato** 100,000 6 300,000 1 800,000 5 800,000 20 2,000,000

Squash 80,000 < 1 100,000 < 1 400,000 5 200,000 5 780,000

Cabbage 60,000 < 1 200,000 5 260,000

Eggplant 6,000 < 1 200,000 45 206,000

Celery 200,000 10 200,000

Artichokes 50,000 5 50,000

Brussels

Sprout**

60,000 30 60,000 45 120,000

> 1

million

pounds

Almonds 100,000 < 1 7,000 < 1 2,500,000 < 1 200,000 < 1 2,807,000

Walnuts 20,000 < 1 5,000 < 1 1,700,000 < 1 100,000 < 1 1,825,000

Cotton 200,000 < 1 1,100,000 < 1 1,300,000

Total

Pounds

Sugar Beets 60,000 < 1 400,000 < 1 700,000 < 1 1,160,000

Grapes 8,000 < 1 7,000 < 1 600,000 < 1 500,000 < 1 1,115,000

*Notes: Crops are grouped using criteria of greater than 5 percent of the crop treated (PCT) of at least one fumigant, greater

than one millions pounds active ingredient used annually of at least one fumigant, or more than a million pounds active

ingredient used of one or more of the soil fumigants. This table does not include values (based on EPA data) for metam

potassium, as follows: Cucumber- 120,000; Onions- 130,000; Peppers- 450,000; Potatoes- 1,300,000; Tomatoes- 350,000;

Watermelon- 450,000 pounds.

Sources: Reference 16

Table data was taken from BEAD Screening Level Usage Analyses (SLUA) unless otherwise indicated.

** Data are from the National Center for Food and Agricultural Policy, 1997 National Pesticide Use Database.

**Data are from the California Department of Pesticide Regulation, 2001 and 2002 Pesticide Use Reporting Database.

P 63 Age Sex Circumstances Symptoms 30 years

i Male Methyl iodide synthesis

Method not specified Latency period not specified Vertigo, ataxia, diplopia. From day 5: agitation, confusion and delirium Gradual recovery starting at day 12

21 months after exposure: Persistent cognitive deficit and personality disturbances

35 yearsii Male Methyl iodide synthesis, from

dimethyl sulfate and sodium iodide Open method: exposure to methyl iodide vapors

Episodes of giddiness and sleepiness On re-exposure: drowsiness, ataxia, dysarthria, nystagmus, strabismus Twitching of the extremities and vomiting; then coma Day 8 after exposure: Death Post-mortem examination: congestion of all organs

34 yearsiii Male Methyl iodide synthesis from

methanol and sodium iodide Open method: exposure to methyl iodide vapors

Symptom-free for 2 days post-exposure Days 3–4: Drowsiness, diplopia, ataxia Days 5–6: Semi-comatose condition with nuchal rigidity, strabismus, and vomiting

Days 7–12: Nystagmus and cerebellar signs with adiadokokinesis, dysmetria, ataxic gait, dysarthria; diffusely abnormal EEG Days 13–60: Gradual disappearance of the neurological symptoms and normalization of the EEG Days 61–99: Psychiatric syndrome with hypochondria,

depression, and insomnia Days 100–121: Progressive recovery

30 yearsiv Male Occupational exposure to methyl

iodide vapors Headache, diplopia, vertigo, ataxia, dysarthria, then agitation, nystagmus, and cerebellar syndrome; diffuse EEG abnormalities Clinical recovery within 5 months but persistence of EEG abnormalities

35 yearsv Male Occupational exposure to methyl

iodide vapors Headache, vertigo, ataxia, dysarthria; then cerebellar syndrome, pyramidal syndrome, hallucinations, and delusions Gradual improvement within 5 months but persistence of hindering neurological sequelae

38 yearsvi Female Occupational exposure to methyl

iodide vapors Contamination of clothes with

liquid methyl iodide

Symptom-free interval of 24 hours Dizziness, weakness Day 3: Diplopia, ataxia, dysarthria, tetraparesis

Day 4: Auditory hallucinations and delusions Gradual improvement within 2 months One year later, persistence of disabling sequelae: ataxia and dysarthria

41 yearsvii

Male Methyl iodide synthesis Method not specified Prolonged exposure to methyl iodide vapors

Dermal contamination (right thumb)

Blurred vision and unsteadiness of gait during exposure Symptomfree interval of a few hours Diplopia, dysarthria, ataxia, dysmetria, nystagmus, confusion, drowsiness

EEG: diffuse slow waves Chemical burn of the contaminated thumb Gradual improvement during the first 3 weeks Then, auditory and visual hallucinations, paranoid ideation, and delusions Gradual recovery within 5 months

Adultviii

Female Handling of methyl iodide with

rubber gloves

Chemical burn of the hands

No systemic reaction

19 yearsix Male Intravenous injection of 6 mL (14

g) methyl iodide Counteracted by administration of N-acetylcysteine

Drowsiness, agitation, hypotension, hyperthermia Metabolic acidosis, hyperleucocytosis Serum methyl iodide concentration: about 60 pg/mL, 3 hours after injection Treatment: Hemoperfusion and N-acetylcysteine administration Complete recovery within 5 days

MeI Risk Characterization


P 82

Table VI: Variability in late resorption data rabbits exposed to MeI by inhalation during gestation days 6

to 28.

Late Resorption Dose (ppm)

0 2 10 20

Number of litters 23 20 20 21

Number of

implantation sites in

each litter

2 to 11 1 to 11 2 to 10 1 to 10

Affected litter 2 2 6 11

Range of % fetus

affected in affected

litter

10.0%

28.6%

16.7%

45.5%

12.5%

to 71.4%

10.1%

to 87.5%

Range of % fetus

affected for all litters

0 to 28.6% 0 to 45.5% 0 to 71.4% 0 to 87.5%

Mean % fetus

affected/litter

1.7±6.2% 3.1±10.7% 11.1±21.2% 21.5±26.9%

P 84

Table VI-8: Reference concentrations for MeI inhalation exposure.

Duration Toxicity endpoints HECs RfCc

UF=30 UF=300

Acute Fetal death in rabbitsix

Worker (8 hr)=0.23 ppm

GPW (24 hr)=0.081 ppm

0.8 ppb

0.3 ppb

Olfactory epithelial

degeneration in ratsix

Worker (8 hr)= 17.1 ppm

Adult (24 hr)= 5.7 ppm

Child (24 hr)= 3.5 ppm

Infant (24 hr)= 2.7 ppm

570 ppb

190 ppb

118 ppb

90 ppb

Neurotoxicity in ratsix





35 ppb

12 ppb

7 ppb

6 ppb

Sub-

chronic

Decreased day 21 body

weight in rat pups

(Nemec, 2002b)ix



17 ppb

13 ppb

Neurotoxicity in rats

(extrapolated)16





12 ppb

4 ppb

2 ppb

2 ppb

Chronic Salivary gland metaplasia

in ratsix





66 ppb

22 ppb

14 ppb

10 ppb

Neurotoxicity in rats

(extrapolated)16





4 ppb

1 ppb

0.7 ppb

0.5 ppb

Lifetime Thyroid tumors in rats15

Non-threshold:

Worker (8 hr)= unit risk 6x10-6

/ppb

GP= unit risk 2.5x10-5

/ppb

Risk benchmarksd:

1.7 ppb

0.04 ppb

Threshold:


GPA= 0.39 ppm

NA

NA

4 ppb

1 ppb


P 106

Table VII-Error! Main Document Only.: Reference Concentration Scenarios

Scenario Worker RfC

(ppb)

Bystand- er RfC

Source Application Method

Conclusions Regarding Mitigation

I 0.8 0.3 DPR

Risk Assess

ors/

SRC/ OEHH

A

Drip · Buffer zones would be “excessive and

difficult to enforce.” “The registrant may find these buffer zones unacceptable due

to its economic viability.”

· Regarding worker protection mitigation for drip application, observing that “the

registrant may find these mitigation measures unacceptable.”

II 8 3 DRP Risk

Managers

Drip, Bedded Shank,

Broad- cast Shank

Regarding worker protection mitigation for shank application, observing that “the


III 15 5 DRP

Risk Manag

ers

Drip, Bedded

Shank, Broad- cast

Shank



IV 30 10

DRP

Risk Manag

ers

Drip, Bedded

Shank, Broad- cast

Shank

Regarding worker protection mitigation for

shank application, observing that “the registrant may find these mitigation measures

unacceptable.”

V 51 17 DRP Risk

Manag

ers

Drip, Bedded Shank,

Broad- cast

Shank

Regarding worker protection mitigation for

shank application, observing that “the registrant may find these mitigation measures

unacceptable.”

VI 96 32 DRP Risk

Managers

Drip, Bedded Shank,

Broad- cast Shank



16

Key industrial toxics

recognized for a

considerable period

“Safe” air concentration of benzene (TLV)

has declined 200-fold in 50 years

0

10

20

30

40

50

60

70

80

90

100

1940 1950 1960 1970 1980 1990 2000

Year

TL

V (

pp

m) ACGIH TLVs for Benzene, 1946 -1997

0.5ppm

100ppm

Benzene recognized

since fifteenth century;

Exposure to benzene

in the air causes

leukemia, a potentially

fatal cancer of the

blood. Including acute

myeloid leukemia or

acute non-lymphocytic

leukaemia.

IARC rated benzene

as "known to be

carcinogenic to

humans"

http://en.wikipedia.org/wiki/Leukemia

http://en.wikipedia.org/wiki/Cancer

http://en.wikipedia.org/wiki/Acute_myeloid_leukemia

http://en.wikipedia.org/wiki/Acute_myeloid_leukemia

ENVIRONMENTAL HEALTH

• “Environmental health comprises those aspects of human health, including quality of life, that are determined by physical, chemical, biological, social, and psychosocial processes in the environment” (WHO).

• The science and knowledge we bring to the looming environmental crises must evolve to enable prevention/control and protection of public health.

THE ENVIRONMENT IS A POWERFUL DETERMINANT OF HEALTH,

As Nations Develop, Patterns of Disease Change Profoundly

• Infectious diseases decline in frequency and severity (AIDS and tuberculosis notwithstanding)

• Life expectancy increases

• Infant mortality declines

• Chronic diseases such as cancer and cardiovascular, become increasingly prevalent

The Epidemiologic Transition

Traditional Diseases,

e.g. infectious

Modern, e.g.

non-communicable

Non-transitional, e.g.,

injuries

Not mortality, i.e., Life span; die later

Environmental Health

• Environmental health problems were local in their effects and short in duration

• Todays problems are persistent and global

• Problems not amenable to quick technical fixes

• Problems require fundamental shift in culture, politics and attitudes; we must change the SOCIAL ENVIRONMENT

• 1970s-Death from coronary heart disease: 1.2 x greater in men in lowest social class

• 1990s-Ratio increased to 2.2

• Today a 3 fold inverse gradient in coronary heart disease mortality

• How do we explain what appears to be class differences?

Environmental successes during the past century?

• What were the key environmental successes during the past century?

– Decline in infectious disease

– Smoking and cancer

– Elimination of lead from gasoline and paint

– Seat belts

– Fluoride in water

•The social environment

Patterns of Disease Change with Development

Environmental Change is the Driving Force

Rates of homicide in Chicago and England and Wales by age and sex of perpetrator; homicide rate is

a reflection of a disorder society-how to change-Given testosterone antagonist?

Emphasis on addressing environmental health problems in terms of media,

constituencies-new areas

•Media –Air –Water –Hazardous waste –Pesticides –Food –Soil

•Constituencies

–Occupational health •Mining •Work environment

•Global issues –Global warming –Ozone depletion –New technologies –Impact of globalization –Population –Climate –Habitat destruction –Biodiversity –Consumption –Resources

•New areas of emphasis

–The built environment –Urban Sprawl –Psychosocial factors –Behavioral issues –Obesity

In utero, children, long term impact

neurological, endocrine disruption

Relevant tools at our disposal for studying sourcehealth effect

• Exposure assessment including physical/chemical characterization of toxic agents

• Structure-activity relationships

• Toxicology including chemical, biological toxicology and in vivo studies

• Epidemiology including genetic epidemiology and molecular epidemiology

• Biological and chemical mechanisms

• Case studies

Policy related issues

• Decisions, decisions decisions-how do we decide whether a chemical is toxic, poses a risk to humans, and what are intervention strategies for control?

• What is the level of proof required for intervention and control to protect public health? Science and policy

• What are the criteria for these decisions? Science and policy

• Need for alternatives analysis

• Example of all this: what is a CARCINOGEN? Once we decide what is our policy for addressing it.

Increases in concentration of lead in Greenland*

*shown on a logarithmic scale.

McMichael, T. (2001). Human frontiers, environments, and disease. Cambridge, UK, Cambridge University Press.

Lead is ubiquitous

Lead is

ubiquitous

Towards Eliminating Childhood Exposure to Lead

Draft

4/63

toxicity of lead, and in developing policies to reduce childhood lead exposure and in managing 1

cases and outbreaks of lead poisoning. The Working Group was tasked with developing 2

guidance for health care authorities, policy makers, health care providers and environmental 3

officers on prevention of childhood lead poisoning. At the closing session of the Informal 4

Workgroup, consensus was reached on five achievable actions for lowering blood lead levels in 5

large populations of children. These actions comprise the core elements of a global strategy to 6

end childhood lead poisoning 7

8

9 10

11

12 To achieve the goal of ending childhood lead poisoning worldwide, this document offers 13

evidence-based guidance for health care authorities, policy makers, health care providers and 14

environmental officers. The document emphasizes the critical importance of primary prevention. 15

The document was developed with consideration of the diversity of scenarios where economics, 16

social issues, resources and community empowerment contribute to barriers and supports. It 17

offers a framework for public health agencies, nongovernmental organizations and field workers, 18

and it touches on the specific needs of these partners. Validated and field tested approaches to 19

addressing environmental lead contamination are described. Variations on the overall approach 20

are modified as appropriate to fit four specific scenarios: 21

22

· Countries/regions that recognize the problem of childhood lead poisoning, that have 23

developed systems for surveillance and prevention, and that have taken interventive 24

action, but where more remains to be done. Experience in these countries shows that 25

pockets of lead poisoning can persist in poor and marginalized communities and that new 26

sources of exposure can continue to appear even as major sources are addressed through 27

strict regulations. 28

· Countries/regions with lead “hot spots" that require urgent intervention (e.g. smelters). 29

· Countries/regions where the problem of childhood lead poisoning is recognized to exist 30

in relation to various sources of exposure, and nation-wide assessment and planning is 31

required, but not yet implemented. 32

· Countries/regions where the problem of lead exposure in children has not been examined 33

or assessed and/or the potential problem is being ignored. 34

35

36

37

38

To end childhood lead poisoning in countries around the world, five achievable actions,

with a proven track record of success in lowering blood lead levels in large populations

of children must be implemented. These are:

1) Complete the removal of lead from gasoline.

2) Ban all other non-essential uses of lead.

3) Remove lead from paint and solder in canned food.

4) Set and enforce enforceable standards for lead in paint, soil, dust, water and air.

5) Establish blood lead levels of concern that are consistent with current science on low-

level lead toxicity in children.


Draft These images are under consideration for inclusion in the draft and require permission from the sources:

Not for Distribution

1/5

Figures and charts

Figure 1 : Source: Norm Healy

Figure 2 (Source: Bruce Lanphear) (Lanphear et al., 2004) (Maybe Bruce has a better

picture graph)


Draft These images are under consideration for inclusion in the draft and require permission from the sources:

Not for Distribution

1/5

Figures and charts

Figure 1 : Source: Norm Healy

Figure 2 (Source: Bruce Lanphear) (Lanphear et al., 2004) (Maybe Bruce has a better

picture graph)

33

Advertisements by National Lead Company from

1923-1935

34

35

Ethyl

Gasoline

Corporation

Ad in

1923

Putting lead in gasoline in the 1920s has been called

“the worst environmental decision of the 20th century.”

Arsenic • Air

– Burning fossil fuels

• Food – Vegetables and fruits (Due to pesticides/herbicides)

– Meat consumption esp. seafood.

• Water – Weathering of Rocks

– Non-ferrous metal smelting

• Soil – Same as water

– Wood preservatives

– California example: Owen’s lake

As. “Hotspots”

2002

Taiwan

Chile Argentina

Arsenic in Bangladesh and West Bengal

• 1970s and 1980s - International aid to drill tube wells and improve water supplies

• 1983 - First skin lesions detected

• Estimated populations exposed:

– Bangladesh: 35-77 million (of 125 million)

– West Bengal: 1.5 million

Hyperkeratosis

Arsenic carcinogenicity by ingestion in drinking water

Comparison of Smith and Cal/EPA

As exp. for risk of 10-3

As exp. for risk of 10-6

(PHG)

Cal/EPA 4 mg/L

4 ppb

0.004 mg/L

4 ppt

Smith 2.5 mg/L

2.5 ppb

0.0025 mg/L

2.5 ppt

History

• First Air Pollution Commission: 1265-1306

– Recommended banning coal in London

– Implementation delayed for ~650 years

– London, UK: 1952 (Smoke + Fog = Smog)-no wind, inversion-stagnant

How small are these particles?

Human Hair

(60 mm diameter)

PM10

(10 mm)

PM2.5

(2.5 mm)

Hair cross section (60 mm)

PM0.1

(0.1 mm)

adsorbed toxics

vapor-phase toxics condensed-phase toxics

Aerosol Toxics

Ultrastructural analysis of lung tissue found inhaled ultrafine

particles were located within the epithelial barriers, cytoplasm,

mitochondria and the nucleus of cells.

Particle Counts in the L.A. Basin Location where measured Particle count – number

of particles per cubic

centimeter

Coastal air 600

San Pedro (near Harbor) 42,000

110 Freeway (area with no

diesel trucks)

135,000

710 Freeway, Long Beach

(high percentage of diesel

trucks

300,000-600,000

710 Freeway, maximum

measured

3,000,000

Credit: Dane Westerdahl, Scott Fruin

Size of sugar cube

Summary: Health effects associated with PM exposure

• Effects on CNS and autonomic nervous system

• Low birth weight/preterm babies

• Increase in asthma and other respiratory disease in children and adults

• Decrease in lung development and function in children

• Atherosclerosis in adults

• Cancer

Findings on Epidemiologic Studies on Carcinogenicity of Diesel exhaust

• More than 40 studies

• These studies have found that long-term occupational exposures were associated with a 40% increase in risk of lung cancer.

• Findings are consistent and unlikely due to chance.

• A causal relationship between occ. diesel exhaust exposure and lung cancer.

• Risk about 1 excess cancer/10,000/ug/m3

MATES-II Assessment of Cancer Risk in LA Basin

Basinwide Cancer Risks* ~1400 in a million

71%

8%

7%

3%

11%

Diesel Particulate

1,3 Butadiene

Benzene

Carbonyls

Other

710 Freeway - Trucks

• Today: 33,000 a day

• 2020: 120,000 a day

• International vehicles not effectively regulated

• What does this about our culture, accidents, noise, air pollution, overall quality of life, walkability, tire debris, particular problems for children

New Cancer Cluster Study USC, School of Medicine

Professor T. M. Mack

• Examines cancer clusters throughout LA county over 25 year period

• Both LA and LB port communities identified having high cancer rates

Deposition and Pathways of Particle Translocation Within and

Outside Respiratory Tract--Main Mechanism for UFP is Diffusion

•Translocation of UFP to

interstitium, capillaries, heart

•Uptake by endothelium; platelets

•Activation/interaction of endothelial

cells, platelets and leukocytes

Alveolar inflammation

Translocation of UFP from

NP and TB region along sensory

neurons to CNS (neurodegeneration)

Un

tre

ate

d

Co

ars

e

M

P P

M

Mag. x 6000 Mag. x 21000

Mag. x 6000 Mag. x 21000

RA

W 2

67

.4

P

P

M

M

M

M

Ultrafines lodge in and destroy mitochondria

Li et al, Environ Health Perspect, 2009

Animal Model to Study PM Effect on Allergic Sensitization

Saline OVA OVA + UFP

H &

E

(Mo

rph

olo

gy)

AB

/PA

S

(Mu

co

su

bsta

nces)

Ma

jor

ba

sic

Pro

tein

(Eo

sin

op

hils

)

Summary

UFP are capable of acting to enhance the primary allergic sensitization response to experimental allergens Inhalation of “real-life” UFP could lead to a profound allergic inflammation deep in the lung in previously sensitized animals

Oxford Street,

London, UK

(Exposure Site)

Hyde Park, London

(Control Site)

Persons with asthma, accompanied by study staff, walking

at Hyde Park site (duration: 2 hours)

Mean and SE of % Change from Baseline for FEV1

0 2 4 6 8 20 22

-10

-8

-6

-4

-2

0

2

% C

ha

ng

e fro

m b

ase

lin

e

Time (hr)

Control Exposure

FEV1, mild asthma

0 2 4 6 8 20 22

-10

-8

-6

-4

-2

0

2

% C

ha

ng

e fro

m b

ase

lin

e

Time (hr)

Control Exposure

FEV1, moderate asthma

d.f=(6, 272) F=0.86 p=0.525 d.f=(6, 244) F=1.84 p=0.093

The reduction in lung function (FEV1 and FVC) was

accompanied by increased airway inflammation We consider inflammation of the lung and heart to be

fundamental issues in disease and illness especially lung and cardiovascular

We have shown the pathway (roadmap) from exposure

to changes in cells to inflammation and health effects

Adverse Effects on Lung Function and Airway Inflammation

Results: More asthma within 150 m of major roads

0

0.5

1

1.5

2

2.5

<75 75-150 150-300 >300

Distance to Major Road (meters)

Asth

ma O

dd

s R

ati

o

McConnell, et. al. AJRCCM 2005;2:A522

Children aged 5-7-lifetime asthma, prevalent asthma, and wheeze

Experimental Design: apoE-/- mice

E-/-

Exposures: 5 hours/session

3x/week for 5 weeks

PM2.5

(FP)

PM0.1

(UFP)

Filtered air

(FA) Non-exposed

(NE)

* Aortic atherosclerosis assessment

Chow

6-week-old male

PM promotes atherosclerosis

Aortic lesions-UFP result in most significant impact with

respect to atherosclerosis

Araujo J, 2008

Aortic atherosclerotic lesions A

ort

ic l

esio

n a

rea (m

m2/s

ecti

on

)

Condition

0

10000

20000

30000

40000

50000

60000

70000

UFP

P= 0.02

P<0.0001

P= 0.002

NE FP FA

P= 0.02

Cardiovascular Health and Air Pollution

Study-Health outcomes.

• Blood Pressure

• Evidence of ischemia-a restriction or thinning in blood supply

• Airway inflammation produces

immunological response and

exacerbation of atherosclerosis

Offshoring: Imported electronic waste, Lianjiang River, Guiyu,

China All China photos copyright 2001, Basel Action Network

Electronic waste recovery workers, Guiyu, China

Toner recovery worker, Guiyu, China

Carbon black (IARC 2A carcinogen); cartridge dumping

Risk assessment

Erin Brockowitch-Carcinogenicity Evidence

• Cr VI is known to cause lung, nasal and/or sinus cavity cancers in humans (30 occupational studies) • There is suggestive evidence of distant tumors in

humans (bladder-stomach) • Key-oral intake-valence state

• Cr VI causes tumors in laboratory animal studies by multiple exposure routes

• Cr VI is genotoxic animals and cells, inducing DNA damage, gene mutation, chromosomal damage

• IARC: “Cr VI is carcinogenic to humans”

Key issue

• “The greater absorption of Cr(VI) than of Cr(III) implies that absorption from the gastrointestinal tract is so rapid that it is able to compete effectively with reduction in the stomach.”

• O’flaherty et al., Toxicological Sciences, 60, 196-213,

2001

Chromium VI and cancer • Results of a study by the National Toxicology Program

• Male and female rats and mice

• Significant increases in tumors at sites rarely seen in lab animals

• Oral cavity and (mice) small intestine (dose-response)

• Chromium VI is a potent human carcinogen, but still widely used-are there alternatives-high priority, why is the State not proactive

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