How much does the environment contribute to cancer? 


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How much does the environment contribute to cancer?



The International Agency for Research into Cancer (IARC) classifies carcinogenic substances into four groups according to the evidence

 

Sufficient evidence is defined as the establishment of a causal relation between exposure to the agent and human cancer.

Limited evidence is defined as the observation of a positive association between exposure to the agent and human cancer, for which a causal interpretation is considered credible, but chance, bias or confounding could not be ruled out with reasonable confidence.

 


 

THE INTERNATIONAL AGENCY FOR RESEARCH INTO CANCER (IARC) CLASSIFICATION:

 

 

Table 1 Carcinogenicity defined by the International Agency for Research into Cancer
Group Definition Used when
  Carcinogenic to humans Evidence is sufficient
2A Probably carcinogenic to humans Limited evidence in humans, and sufficient evidence in experimental animals,
2B Possibly carcinogenic to humans Limited evidence in humans, and absence of sufficient evidence in experimental animals, or
  Inadequate evidence in humans or human data non-existent and sufficient evidence in experimental animals
  Not classifiable as to carcinogenicity to humans Not classifiable to any other group
  Probably not carcinogenic to humans Evidence suggests a lack of carcinogenicity in humans and in experimental animals

 

Researchers suggest that lung cancer, in particular, may be increased by ambient air pollution, chiefly due to the incomplete combustion of fossil fuels.

A considerable number of studies have compared lung cancer rates in urban and rural residents of the same country, and have showed increased incidence in urban areas.

This relationship has been further explored in a series of studies of changes in lung cancer experience of immigrants to various countries. For example, several investigations on emigrants from the UK to New Zealand showed that, in general, the lung cancer rates of emigrants were lower than that of residents in the UK but higher than those born in the new country.

Some environmental studies have indicated that lung cancer is more closely related to sulfates (IARC –?). Other constituents of air that have been associated with increased lung cancer include asbestos (IARC - 1), polycyclic hydrocarbons (IARC - 1), and diesel exhaust (IARC -?).

The evaluation of the role of air pollution in the aetiology of other cancers is even more equivocal than for lung cancer. Associations have been suggested, for example, with digestive and gastrointestinal tract cancers, bladder cancer, oesophageal cancer, and breast cancer.

 

 

Children's Vulnerability to Air Pollution

Respiratory health

Numerous studies have reported adverse effects of air pollution on the respiratory health of children, using indicators of general air pollution and of traffic-related air pollution.

In Europe, studies have found that more than 10% of children ages 13-14 suffer from asthma, with a significant burden of disease attributable to outdoor air pollution.

Some studies have investigated the expected beneficial effects of air pollution reduction on respiratory health in children. In cross-sectional analysis, the tremendous decline of coal combustion-related air pollution in East Germany after reunification was associated with a decline of respiratory symptoms and improved lung function in children. In a cohort of children, those who moved within California to areas with lower PM10 levels showed increased lung function growth, whereas those moving to more polluted areas had a decreased growth. A rather moderate decline of air pollution levels in the 1990s in Switzerland was associated with a reduction in respiratory symptoms and diseases in school children.

Blood lead levels

In the last decade children’s blood lead levels have fallen significantly in a number of countries. Despite this reduction, childhood lead poisoning continues to be a major public health problem for certain at-risk groups of children, and concerns remain over the effects of lead on intellectual development in infants and children. The evidence for lowered cognitive ability in children exposed to lead has come largely from prospective epidemiologic studies.

The main sources of lead in children’s environments are diet, lead-based paint in older housing, lead in soil and dust from contaminated leaded paint and gasoline, or past and present mining and industrial activity. Exposure from air and waterborne sources has been greatly reduced with the introduction of unleaded gasoline and the replacement of lead water pipes and water tanks with nonlead alternatives. However, lead in soil and dust continues to be a major source of exposure.

 

Three groups of reasons, which can explain children's vulnerability to air pollution, should be mentioned:

1. Behavioral reasons: Younger children are often unaware of health risks around them and are typically unable to make choices to reduce their risk. For example, hand to mouth behavior, typical of very young children, exposes them to lead dust and other harmful substances deposited from the air.

2. Physiological reasons: Children breathe more air than adults do in proportion to their body weight. Children also react to certain toxicants more severely than adults because of their narrower air passages and their smaller size. Given their small stature, children's breathing zones are closer to the ground which can expose children to high concentrations of air pollutants.

3. Developmental reasons: Children's lungs are growing rapidly during the first year of life and they continue to develop air sacs through their first four years. Exposure to air pollutants during these formative years could hinder normal lung development. The developing nervous system is thought to be far more vulnerable to the toxic effects of lead than the mature brain.


 

Pregnancy outcomes

The study of birth outcomes is an important emerging field of environmental epidemiology.

Birth outcomes are important in their own right because they are important indicators of the health of the newborns and infants.

In addition, low birth weight (LBW), intrauterine growth retardation (IUGR), and impaired growth in the first years of life are known to influence the subsequent health status of individuals, including increased mortality and morbidity in childhood and an elevated risk of hypertension, coronary heart disease, and non-insulin-dependent diabetes in adulthood.

I’d like to present you the review on the evidence linking adverse birth outcomes with ambient air pollution.

The birth outcomes have been divided into five groups: a) mortality of fetuses and infants, b) LBW, c) premature (preterm) births, d) IUGR, and e) birth defects.

The evidence is sufficient to infer a causal relationship between air pollution and respiratory deaths in the postneonatal period. The studies found an association between sulfur dioxide and total suspended particles and respiratory mortality in the postneonatal period.

For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants (particular matters, sulfur dioxide, carbon monoxide, nitrogen oxides).

For preterm births and intrauterine growth retardation (IUGR), as well as birth defects, the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies.

Molecular epidemiologic studies suggest possible biologic mechanisms for the effect of air pollution on birth weight, premature birth, and IUGR. It has been shown that the levels of DNA adducts are positively related to risk of IUGR, birth weight, birth length, and head circumference, and hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus mutation frequency in infants.

In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.


Ambient air pollution and pregnancy outcomes: a review of the literature

by Radim J. Sram, Blanka Binkova, Jan Dejmek and Martin Bobak

Environmental Health Perspectives April 2005 v113 i4 p375(8)

OUTCOME EVIDENCE POLLUTANTS
respiratory deaths in the postneonatal period sufficient - sulfur dioxide, - total suspended particles
birth weight suggests causality needed to confirm the role of different pollutants: - particular matters, - sulfur dioxide, - carbon monoxide, - nitrogen oxides
preterm births insufficient  
intrauterine growth retardation insufficient  
birth defects insufficient  

Air pollution control

Practically, all countries have adopted legislation /regulation.

Policy objectives

STANDARDS AND MEASUREMENTS

RUSSIAN FEDERATION

In Russian Federation air quality is evaluated in reference to the former Soviet Union reference values (the state standards). These include more than one thousand pollutants.

The standards are called maximum allowable concentrations (MAC), and mainly consist of short-term (20 to 30 minutes) or daily average concentrations.

Generally, MACs are stricter than WHO guidelines, except for some heavy metals or PM.

Vehicles emissions are also subject to state standards, which have not been revised since Soviet times, and are less strict than any EU or UN/ECE or United States standards.

 

WHO AIR QUALITY GUIDELINE:

 

Pollutant Averaging time AQG value
Particulate matter PM2.5     PM10   1 year 24 hour (99thpercentile)   1 year 24 hour (99thpercentile)     10 µg/m3 25 µg/m3   20 µg/m3 50 µg/m3
Ozone, O3   8 hour, daily maximum 100 µg/m3  
Nitrogen dioxide, NO2   1 year 1 hour   40 µg/m3 200 µg/m3
Sulfur dioxide, SO2   24 hour 10 minute 20 µg/m3 500 µg/m3

 

 

The most relevant instruments for compliance and enforcement of clean air policy objectives are (PRINTOUT16):

1. licensing polluting activities;

2. inspection;

3. economic instruments;

4. and monitoring activities.

Policy instruments



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