2. What Is Cumulative Risk Assessment?
3. Vulnerability in the Context of Cumulative Risk Assessment
3.1. Susceptibility and Sensitivity (Vulnerability Related to Biological Characteristics)
3.2. Differential Exposure (Vulnerability Related to an Increased Chemical Burden)
3.3. Differential Preparedness and Recovery (Vulnerabilities Related to Social Environment and Behavior)
4. Cumulative Risk Assessment and the Traditional Risk Assessment Paradigm
4.1. Hazard Identification
4.1.1. Physical and Biological Stressors
4.1.2. Social Stressors
4.2. Exposure Assessment
4.4. Risk Characterization
4.5. Risk Management
5. Non-Chemical Stressors and Air Pollution Exposures
5.1. Animal Studies Examining the Cumulative Effects of Exposure to Chemical and Non-Chemical Stressors
5.2. Epidemiological Studies Examining the Cumulative Effects of Exposure to Air Pollutants and Non-Chemical Stressors
18.104.22.168. Short-term Studies
22.214.171.124. Long-term Studies
126.96.36.199. Cardiovascular Effects
188.8.131.52. Neurological Effects
184.108.40.206. Asthma and Other Respiratory Health Effects
220.127.116.11. Limitations Associated with the Use of Epidemiological Data
6. Research Needs and Conclusions
- Identification of the elements of low SES that have the most significant impact on disease (e.g., to what relative extent does poor nutrition vs. psychosocial stress vs. lack of quality healthcare play a role in disease), investigated on a disease-specific basis.
- Metrics to describe degrees of psychosocial stress and other key biological effects of non-chemical stressors, specifically expressing non-chemicals stressors in manner where “dose”-response relationships can be explored.
- Correlations between gross measures of exposure (e.g., the presence of a landfill) and actual chemical exposure in a population.
- Biomarkers that are reliable indicators of the cumulative effects of chemical and non-chemical stresses.
- Correlations between stress induced in animals and psychosocial stress in humans, specifically whether these animal stress models are applicable to human conditions.
- Quantification of the interactions between non-chemical stressors and chemicals and their relative role in health outcomes. Specifically, how dose-response curves change with combined exposures to chemical and non-chemical stressors.
- Epidemiological evaluations specifically designed to explore the relative contribution of chemicals and non-chemical stressors in disease outcomes, and, specifically, how observations relate to dose-response relationships.
- Focused efforts to better “link” research on dose-response relationships to observations gleaned from epidemiological evaluations.
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|Criteria air pollutant||Susceptibility factors||Other vulnerability factors||Reference|
|Carbon monoxide||Pre-existing disease|
|Differential exposure/dose (e.g., altitude, exercise, proximity to roads)|
Abuse of medication and other substances
SES (e.g., education and income)
|Particulate matter (PM10 and PM2.5)||Pre-existing disease|
|SES (e.g., education, unemployment, and income)|||
|Differential exposure (e.g., activity level, time spent outdoors; physical activity)|
SES/racial ethnic factors (e.g., education and income)
Environmental factors (urban vs. rural, ETV, endotoxin exposure)
Physiological states (menopause, pregnancy, lactation)
|SES (e.g., education, life stress, and income)|||
|Sulfur dioxide||Genetic factors|
|SES (e.g., education and income)|
Differential exposure (e.g., activity level, residential location, AC use, time spent outdoors)
|Nitrogen dioxide||Pre-existing disease|
|SES (e.g., education and income)|
Differential exposure (e.g., proximity to roads)
|Selected potential indicators of vulnerability (individual)||Selected potential indicators of vulnerability (community)|
|Susceptibility and sensitivity (biological characteristics)||Inherited diseases/predisposition to disease|
|Mental health (coping skills)|
|Low birth weight|
|Differential exposure (increased chemical burden)||Old, substandard housing||Old, substandard housing|
|Cleanliness/sanitation||Inadequate air flow|
|Home use of pesticides||Increased air pollutant exposure|
|Substandard hygiene||Traffic density|
|Poor ventilation||Proximity to hazardous waste sites|
|Proximity to waste disposal sites|
|Proximity to industrial releases|
|Differential preparedness and recovery (social environment and behavior)||SES||SES|
|Family instability||Crime and violence|
|Personal nutrition||Lack of community resources|
|Smoking||Access to quality health care|
|Drug addiction||Substandard schools|
|Chronic underemployment||Concentration of poverty|
|Other aspects of psychosocial stress||Racial segregation|
|Health care access||Noise|
|Health behaviors||Civil engagement/political empowerment|
|Reproductive events||Social capital|
|Draft CalEPA Cumulative Impacts Assessment ||NJDEP Preliminary Screening Method to Estimate Cumulative Environmental Impacts ||NJDEP Strategies for Addressing Cumulative Impacts in Environmental Justice Communities ||US EPA’s NJSEAT |
|Measures of Sensitive Population and Social Indicators|
|Sensitive Populations||None||Social Determinants||Social Demographic Indicators|
|% of population under age 5||Age of housing||% of population living in poverty|
|% of population over age 65||Proportion of population who are children||% of population counted as minority|
|SES||Proportion of population over age 60||% of population 25 years old and|
|% Non-white residents||Poverty rate||over without a high school diploma|
|Median household income||Median family income||% of population over 65 years of age|
|% of residents living below 2X||Racial and ethnic composition of population||% of population under 5 years of age|
|National Poverty Level||Unemployment rate||% of population of limited English proficiency|
|Some measure of parks/recreational space|
|Measures of Environmental Exposure Burden|
|Exposures||Exposures||Pollution burden||Environmental indictors|
|PM2.5 concentrations||NATA cancer risk||Lead in blood of children age 6 or younger||NATA cancer risk|
|Ozone concentrations||NATA diesel exposure||RCRA sites||NATA non-cancer risk|
|Releases from industrial facilities (TRI data)||Estimated benzene emissions||TRI||NATA non-cancer diesel PM|
|Traffic (all)||US EPA National Priorities List sites||Toxic chemical emissions and transfers from industrial facilities|
|Traffic (trucks)||Power plants|
|Density of major regulated sites||Treatment, storage, and disposal facilities||Population-weighted ozone monitoring data|
|Density of known contaminated sites||Brownfields|
|Density of dry cleaners||Known contaminated sites||Population-weighted PM2.5 monitoring data|
|Density of junkyards||Municipal incinerators|
|Resource recovery landfills|
|Incinerator ash landfills|
|Sewage treatment plants|
|Municipal solid waste landfills|
|Trash transfer stations|
|Environmental effects||Compliance indicators|
|Hazardous waste and cleanup sites||Inspections of major facilities|
|Leaking underground fuel tanks||Violations at major facilities|
|Formal actions at major facilities|
|Facility density based on all facilities in US EPA’s facility registry system|
|Measures of Existing Public Health Problems|
|Public health||Existing health problems||Human health indictors|
|Low birth weight||Total cancer incidence rate||% infant mortality|
|Cancer mortality rate||Total cancer death date||% low birth weight births|
|Asthma hospitalization rate||Asthma: hospitalization rate|
|Asthma: emergency department visits|
|Chronic lower respiratory disease|
|Carbon monoxide poisonings|
|All-cause mortality rate|
|Coronary heart disease rate|
|Low birth weight rate|
|Infant mortality rate|
|Birth defect rate|
|Some measure of violence/crime|
|Availability of preventive services|
|Childhood lead screening rate|
|Total population of census tract|
|Size (area) of census tract|
|Health outcome||Chemical stressor||Non-chemical stressor||Results||Reference|
|Short-term studies||CoH (PM indicator); SO2||SES indicators: unemployment, poverty, education, high manufacturing employment||Effect modification by SES measures; slightly higher relative risks and more significant results across the lag periods tested|||
|PM2.5||SES indicators: household income, poverty, education||Effect modification only significant for household income|||
|PM10 adjusted for O3, SO2, NO2, CO||SES indicators: education, annual income||No effect modification by SES|||
|PM10||SES indicator: education||Evidence of weak effect modification by education|||
|PM10||SES indicators: unemployment, poverty level, education||No effect modification by SES|||
|PM10, O3||SES indicator: sociospatial development index (based on homes with electricity, homes with piped water and drainage, literacy, and indigenous language speakers)||PM10 not associated with mortality; ozone was significantly associated with mortality, but no consistent effect modification observed|||
|PM10||SES indicators: education, income, living in slums||Effect of PM on respiratory mortality was negatively correlated with % college education, % family income > $3,500, living in slums|||
|PM10||SES indicator: composite index||Larger effect in higher SES areas but not statistically significant|||
|TSP, CO, NO2, SO2, O3, PM10, CoH, PM10–2.5||SES indicator: income||Only NO2 was associated with mortality in low income groups|||
|Short-term studies||PM10||SES indicator: education||Larger mortality risk estimates were observed in least-educated for all cause, respiratory, and heart disease-related mortality|||
|PM10||SES indicator: income, index that includes education, occupation, unemployment rate, family size, crowding, home ownership||The PM10-mortality association was greater in lower income and lower SES communities|||
|O3||SES indicator: education, income, unemployment, poverty||Effect modification only for unemployment; higher mortality rates for higher unemployment|||
|Long-term studies||PM2.5, sulfates||SES indicator: education||Significant effects for both PM2.5 and sulfates in least educated|||
|PM2.5, sulfates||SES indicator: education||Patterns are similar to previous study but effect modification is less clear; for ischemic heart disease pattern was reverse (most educated has greatest risk)|||
|TSP, BS, NO2||SES indicator: education||No effect modification by educational attainment|||
|BS||SES indicator: education||No effect modification by educational attainment|||
|TSP, SO2||SES indicator: income||Relative risks were higher for the low household income category|||
|Air pollution index: sum of standardized measures of TSP and SO2||Deprivation index (includes unemployment and education)||No effect modification|||
|Neurological effects||Blood lead||SES indicator: income||Cognitive deficits (Kaufman Assessment Battery) associated with neonatal blood lead only in poorer families|||
|Blood lead||SES indicator: income||No modifying effect of SES on blood lead-learning/IQ association, but observed trend of greater vulnerability in lower SES subgroup|||
|Blood lead||SES indicator: parents’ occupational prestige||Modifying effects by SES were observed for IQ and blood lead, but interaction became non significant when adjusted for other factors (age at testing, iron status, birth weight, etc.)|||
|Blood lead||SES indicator: composite index including education and father’s occupation||Effect modification of lead-related decreased performance in visual-motor integration and choice reaction tests|||
|Blood lead||SES indicators: Hollingshead’s Four-Factor Index of Social Class, a measure of parents’ occupational and educational achievements||Modifying effects by SES were observed for Mental Development Index and blood lead only at ages 18 to 24 months|||
|Bone lead||SES indicators: neighborhood psychosocial hazards (neighborhood violent crimes, 911 calls, etc.)||Psychosocial stress exacerbated effects of lead on 3 of 7 cognitive measures|||
|Cardiovascular Disease||Lead (bone lead)||SES indicators: stress (based on standardized questionnaire and self-reported)||Effects of lead on hypertension were more pronounced in stressed individuals|||
|O3, CO, NO2||SES indicators: education, income||No effect modification by SES on cardiac hospital admissions|||
|Asthma and other respiratory diseases||NO2 (proxy for traffic)||SES indicators: exposure to violence||Elevated risk of developing asthma with increased NO2 exposure only in children with higher exposure to violence|||
|Traffic-related air pollution (Nitrogen Oxides)||SES indicators: parental education, parental stress||High parental stress was associated with higher incidence of traffic-related risk of developing asthma. An increased risk of asthma was also observed for low SES families exposed to air pollution|||
|O3, SO2, NO2||SES indicators: education, income||Greater hospitalizations for respiratory effects in lower education and lower income strata|||
|NO2, SO2, O3, CO||SES indicator: average household income adjusted for household size||Male children had higher asthma hospitalizations in low SES group with exposure to NO2; female children had higher asthma hospitalizations for SO2 in the low-income group. No associations for O3 or CO|||
|NO2||SES indicator: insurance status||Children without insurance had higher risk of asthma admissions than those with private insurance|||
|PM10, O3, sulfates, strong acidity||SES indicator: insurance status||The overall hospital admissions association for both O3 and PM10 was driven by the uninsured minority population|||
|NO2||Life stress||Greater inflammatory markers associated with high stress in low pollution exposure group|||
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