This article challenges the idea that cancer cannot be prevented among older adults by examining different aspects of the relationship between age and cancer. Although the sequential patterns of aging cannot be changed, several age-related factors that contribute to disease risk can be. For most adults, age is coincidentally associated with preventable chronic conditions, avoidable exposures, and modifiable risk behaviors that are causally associated with cancer. Midlife is a period of life when the prevalence of multiple cancer risk factors is high and incidence rates begin to increase for many types of cancer. However, current evidence suggests that for most adults, cancer does not have to be an inevitable consequence of growing older. Interventions that support healthy environments, help people manage chronic conditions, and promote healthy behaviors may help people make a healthier transition from midlife to older age and reduce the likelihood of developing cancer. Because the number of adults reaching older ages is increasing rapidly, the number of new cancer cases will also increase if current incidence rates remain unchanged. Thus, the need to translate the available research into practice to promote cancer prevention, especially for adults at midlife, has never been greater.
The relation between air pollution and the exacerbation of childhood asthma was studied in a panel of 71 children (aged 5 to 7 yr) with mild asthma who resided in the northern part of mexico City. During the follow-up, ambient measures of particulate matter less than 10 microns (PM10, 24-h average) and ozone (1-h maximum) frequently exceeded the Mexican standards for these contaminants. The peak expiratory flow rate (PEFR) was strongly associated with PM10 levels and marginally with ozone levels. Respiratory symptoms (coughing, phlegm production, wheezing, and difficulty breathing) were associated with both PM10 and ozone levels. An increase of 20 micrograms/m3 of PM10 was related to an 8% increase in lower respiratory illness (LRI) among children on the same day (95% confidence interval [CI] = 1.04-1.15), and an increase of 10 micrograms/m3 in the weekly mean of particulate matter less than 2.5 microns (PM2.5) was related to a 21% increase in LRI (95% CI = 1.08-1.35). A 50 parts per billion (ppb) increase in ozone was associated with a 9% increase in LRI (95% CI = 1.03-1.15) on the same day. We concluded that children with mild asthma are affected by the high ambient levels of particulate matter and ozone observed in the northern part of Mexico City.
Significant increases in asthma morbidity and mortality in the United States have occurred since the 1970s, particularly among African-Americans. Exposure to various environmental factors, including air pollutants and allergens, has been suggested as a partial explanation of these trends. To examine relations between several air pollutants and asthma exacerbation in African-Americans, we recruited a panel of 138 children in central Los Angeles. We recorded daily data on respiratory symptoms and medication use for 13 weeks and examined these data in conjunction with data on ozone (O3) nitrogen dioxide (NO2), particulate matter (PM10 and PM2.5), meteorological variables, pollens, and molds. Using generalized estimating equations, we found associations between respiratory symptom occurrence and several environmental factors. For example, new episodes of cough were associated with exposure to PM10 (OR = 1.25; 95% CI = 1.12-1.39; interquartile range [IQR] = 17 microg/m3, 24-hour average), PM2.5 (OR = 1.10; 95% CI = 1.03-1.18; IQR = 30 microg/m3, 12-hour average), NO2, and the molds Cladosporium and Alternaria, but not with exposure to O3 or pollen. The factors PM10 and O3 were associated with the use of extra asthma medication. For this population several bioaerosols and air pollutants had effects that may be clinically significant.
Spatial variations in mortality and incidence by type of cancer demonstrated both persistent and emerging challenges for cancer control in AI/AN populations.
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