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26 Jul 2019

One of the major goals of toxicology is to predict risk to humans from exposure to chemicals. This involves the processes of risk assessment and risk management. You are the director of a chemical factory and are planning to bring a new chemical to market. Outline the process by which you would develop a risk assessment/management plan for this chemical to assure it safety to humans from exposure.

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Deanna HettingerLv2

27 Jul 2019

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Suppose you live in a community that is being affected by a hazardous chemical from a factory located in the neighborhood. The local health department has conducted a formal risk assessment and has documented peopleâs high levels of exposure to this chemical. Several cases of adverse health effects have been reported to the health department. Previous research has documented that this chemical is a potent neurotoxin. Children are particularly vulnerable to the effects of this chemical. In your own opinion, what steps might be taken for risk management with regard to this exposure?

In epidemiology 101

Can anyone help me with the following questions, it is due tonight and im having a hard time figuring most of these out and in-between a couple of answers. Thanks!

1. Which of the following is the PRIMARY goal of risk assessment?

A. maximize profit

B. balance risks and benefits

C. reduce liability

D. determine lethal doses

2. The probability of an adverse outcome based on the exposure and potency of a hazardous agent is known as the:

A. toxicity

B. risk

C. hazard

D. margin of safety

E. therapeutic index

3. Risk Assessment includes all the following, except:

A. risk characterization

B. exposure assessment

C. dose-response assessment

D. hazard identification

E. cost-benefit analysis

4. The process of making risk information understood by local officials, community groups and other stakeholders is known as:

A. risk management

B. risk characterization

C. risk communication

D. risk perception

E. risk estimation

5. The Hazard Identification step in the risk assessment paradigm may include which of the following:

A. in vitro testing

B. structure-activity relationships

C. animal bioassays

D. epidemiologic data

E. all of the above

6. A basic premise of carcinogen risk assessment is that:

A. surface area is proportional to body weight

B. chemicals that cause tumors in animals will cause tumors in humans

C. all dosing regimens are equivalent

D. all animal strains are relevant

7. The Point of Departure (POD) for a low-dose extrapolation could be which of the following:

A. NOAEL

B. LOAEL

C. BMDL

D. none of the above

E. all of the above

8. The benchmark dose (BMD) approach is preferred over the NOAEL/LOAEL approach for all the following reasons, except:

A. the full dose-response curve is considered

B. it includes a measure of variability

C. the same benchmark response be used across studies

D. it results in lower reference values

9. A biochemical change, functional impairment, or pathologic lesion affecting an organismâs performance, and reducing its ability to respond to environmental challenges is known in risk assessment as the

A. point of departure

B. benchmark dose

C. adverse effect

D. carcinogenic effect

10. When there is a cancer risk of 1 in 10,000, this is considered to be of

A. high concern

B. moderate concern

C. somewhat low concern

D. no concern at all

11. Which toxicant is commonly found in indoor air due to off-gassing of plywood and furniture?

A. arsenic

B. lead

C. methylene chloride

D. dioxin

E. formaldehyde

12. Which if the following was NOT an event in the United States that triggered widespread awareness of environmental issues in the 1960s?

A. Relocation of families from Love Canal in Niagara Falls, NY

B. Cuyahoga River catching on fire in Ohio

C. Publication of Silent Spring by Rachel Carson

D. Nationwide federal ban of smoking cigarettes in bars and restaurants

13. The study of the fate and effects of chemicals in the environment is the definition of: A. Environmental toxicology

B. Ecotoxicology

C. Environmental health toxicology

D. Risk assessment

14. An example of an area source of air emissions would be:

A. A volcano

B. A moving car

C. A gas station

D. A power plant

15. Which of the following is considered to be âgood up high and bad nearbyâ?

A. Ozone

B. Carbon monoxide

C. Carbon dioxide

D. Sulfur dioxide

16. Which of the following water disinfectants is safest from the perspective of not producing any known DBPs?

A. Chlorine

B. Chloramine

C. Ozone

D. UV

17. The most significant anthropogenic source of carbon monoxide would be classified as a:

A. Point source

B. Area source

C. Mobile source

D. Natural source

18. According to Genius (2006), what do some scientists believe is the most frequent cause of childhood cancer and leukemia?

A. Pharmaceuticals in drinking water

B. Exposure to diuretics in utero

C. Prenatal exposure to carbon monoxide and other industry emissions

D. Neonatal exposure to polyvinylchloride (PVC) plastic

19. In the Genius (2006) article, what did the scientists who published in the journal Science discover about the possible transgenerational impact of exposure to environmental toxicants in pregnancy?

A. Epigenetic mechanisms may permanently alter the germ-line and genetic traits of offspring of an exposed individual

B. Epigenetic changes die out after three successive generations of offspring

C. Epigenetic changes only occur when a toxicant is an endocrine disruptor

D. Epigenetic changes never take place when the toxicant is a pesticide or fungicide

20. According to the article by Chemnick and Climatewire (2013), âSoggy Vancouver Island in British Columbia has become an unlikely new home for Cryptococcus gattii, a tropical and subtropical yeast-based fungus.â What health effect does this yeast-based fungus have on humans when it is inhaled?

A. None

B. Triggers asthma attacks

C. Causes a kind of meningitis

D. Eventually leads to lung cancer

greykangaroo345

I'm working on the following problem and would like some help. The current expert answer on here does not even match the problem:

Situation

Native Americans use forest plant species for food and ceremonial purposes. What is the risk to them if some areas of the US national forests and wildernesses where they collect these plants are sprayed with L7, a broadleaf and shrub herbicide?

Background

L7 is a systemic herbicide used to control deeply rooted herbaceous weeds and woody plants in rights-of-ways, forestry, rangelands, pastures, and small grains. L7 has been used for nearly 40 years. In forestry applications, as much as 1 lb active ingredient/acre of liquid is sprayed broadcast on foliage to open wildlife areas and rights-of-way. Only 1 treatment per year is allowed. Reentry into sprayed areas is allowed immediately after drying. Aerobic soil half-life is about 100 days.

Steps: Tier 1 Hazard and Dose-response Data

An acute oral LD50 evaluation was conducted in the rat. The LD50 was greater than 5000 mg/kg BW, so acute exposures are considered practically nontoxic. In a chronic toxicity feeding study conducted in the F344 rat, L7 was evaluated at 0, 20, 60 or 200 mg/kg BW/day for 2 years. The chronic toxicity LOEL was 60 mg/kg BW/day as evidenced by altered size and tinctorial properties of centrilobular hepatocytes and increased absolute and/or relative liver weights in both sexes. The Agency has classified L7 as Group E (evidence of non-carcinogenicity for humans). There is no evidence, based on the available data, to suggest that the chemical was associated with significant reproductive or developmental toxicity under the testing conditions.

A reference dose (RfD) for L7 was calculated to be 0.20 mg/kg BW/day based on a NOEL of 20 mg/kg BW/day from a two-year rat chronic feeding study. An uncertainty factor of 100 was used to account for the inter-species extrapolation and intra-species variability. The L7 chronic dietary exposure/risk estimates are extremely low. Because the dietary exposure/risk is so low, about 1/200th of the RfD, there are no concerns regarding chronic dietary exposure to L7.

Residue

Based on the application rate and the foliage type, the highly conservative estimated environmental residue is 135 mg/kg dry weight immediately after application.

Dietary Exposure

Consumption data on these forest plant species by Native Americans are lacking.

Risk Characterization Assumptions

â¢ Max rate = 1 lb active ingredient/acre

â¢ Body Weight = 70 kg (standard adult male weight used by US EPA)

â¢ Chronic reference dose (RfD) = 0.2 mg/kg BW/d (this is the acceptable daily intake)

â¢ Residue estimate = 135 mg/kg dry weight

â¢ Adult enters the area immediately after spray dries

â¢ Dietary Risk Quotient = Exposure Ã· Toxic Endpoint, so for this example Dietary Risk = (Residue * Consumption Rate) Ã· RfD

â¢ Remember that a risk quotient (RQ) of 1 is where the exposure equals the toxic endpoint.

Questions

a. Given that specific consumption data are lacking for the treated plants, how would you estimate risk to Native Americans from consuming plants containing L7 residue?

b. The total vegetable consumption estimate per day in the US = 0.294 kg/70 kg adult (wet weight), or 0.06 kg/70 kg adult (dry weight). How can you use these numbers to help characterize the risk?

c. What refinements could be made to this dietary assessment?

d. What data elements are needed for higher-tiered aggregate assessments? Aggregate exposures include all possible routes and pathways of exposure to one chemical.