Background Infectious diseases may rival cancer, heart disease, and chronic lung disease as sources of morbidity and mortality from smoking. We reviewed mechanisms by which smoking increases the risk of infection and the epidemiology of smoking-related infection, and delineated implications of this increased risk of infection among cigarette smokers. Methods The MEDLINE database was searched for articles on the mechanisms and epidemiology of smoking-related infectious diseases. English-language articles and selected cross-references were included. Results Mechanisms by which smoking increases the risk of infections include structural changes in the respiratory tract and a decrease in immune response. Cigarette smoking is a substantial risk factor for important bacterial and viral infections. For example, smokers incur a 2- to 4-fold increased risk of invasive pneumococcal disease. Influenza risk is severalfold higher and is much more severe in smokers than nonsmokers. Perhaps the greatest public health impact of smoking on infection is the increased risk of tuberculosis, a particular problem in underdeveloped countries where smoking rates are increasing rapidly. Conclusions The clinical implications of our findings include emphasizing the importance of smoking cessation as part of the therapeutic plan for people with serious infectious diseases or periodontitis, and individuals who have positive results of tuberculin skin tests. Controlling exposure to secondhand cigarette smoke in children is important to reduce the risks of meningococcal disease and otitis media, and in adults to reduce the risk of influenza and meningococcal disease. Other recommendations include pneumococcal and influenza vaccine in all smokers and acyclovir treatment for varicella in smokers.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/217624/ira30766.pdf

Cigarette smoking and infection.

The authors investigated whether neighborhood socioeconomic characteristics are associated with coronary heart disease prevalence and risk factors, whether these associations persist after adjustment for individual-level social class indicators, and whether the effects of individual-level indicators vary across neighborhoods. The study sample consisted of 12,601 persons in four US communities (Washington County, Maryland; Forsyth County, North Carolina; Minneapolis, Minnesota; and Jackson, Mississippi) participating in the baseline examination of the Atherosclerosis Risk in Communities Study (1987-1989). Neighborhood characteristics were obtained from 1990 US Census block-group measures. Multilevel models were used to estimate associations with neighborhood variables after adjustment for individual-level indicators of social class. Living in deprived neighborhoods was associated with increased prevalence of coronary heart disease and increased levels of risk factors, with associations generally persisting after adjustment for individual-level variables. Inconsistent associations were documented for serum cholesterol and disease prevalence in African-American men. For Jackson African-American men living in poor neighborhoods, coronary heart disease prevalence decreased as neighborhood characteristics worsened. Additionally, in African-American men from Jackson, low social class was associated with increased serum cholesterol in "richer" neighborhoods but decreased serum cholesterol in "poorer" neighborhoods. Neighborhood environments may be one of the pathways through which social structure shapes coronary heart disease risk.

Neighborhood Environments and Coronary Heart Disease: A Multilevel Analysis

The role of smoking as a risk factor for periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of periodontitis was markedly higher among current smokers compared with never smokers (P or = 4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the periodontitis in the 19 to 30 year old group and 32% of the periodontitis in the 31 to 40 year old group, is associated with smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for Cigarette Smoking as a Major Risk Factor for Periodontitis

Changes in documented risk factors for breast cancer and rates of screening cannot completely explain recent increases in incidence or mortality. Established risk factors for breast cancer, including genetics, account for at best 30% of cases. Most of these risk factors can be linked to total lifetime exposure to bioavailable estrogens. Experimental evidence reveals that compounds such as some chlorinated organics, polycyclic aromatic hydrocarbons (PAHs), triazine herbicides, and pharmaceuticals affect estrogen production and metabolism and thus function as xenoestrogens. Many of these xenoestrogenic compounds also experimentally induce mammary carcinogenesis. Recent epidemiologic studies have found that breast fat and serum lipids of women with breast cancer contain significantly elevated levels of some chlorinated organics compared with noncancer controls. As the proportion of inherited breast cancer in the population is small, most breast cancers are due to acquired mutations. Thus, the induction of breast cancer in the majority of cases stems from interactions between host factors, including genetics and environmental carcinogens. We hypothesize that substances such as xenoestrogens increase the risk of breast cancer by mechanisms which include interaction with breast-cancer susceptibility genes. A series of major epidemiologic studies need to be developed to evaluate this hypothesis, including studies of estrogen metabolism, the role of specific xenoestrogenic substances in breast cancer, and relevant genetic-environmental interactions. In addition, experimental studies are needed to evaluate biologic markers of suspect xenoestrogens and biologic markers of host susceptibility and identify pathways of estrogenicity that affect the development of breast cancer. If xenoestrogens do play a role in breast cancer, reductions in exposure will provide an opportunity for primary prevention of this growing disease.(ABSTRACT TRUNCATED AT 250 WORDS)

/pdf/medical-hypothesis-xenoestrogens-as-preventable-causes-of-989nq3q8c5.pdf

Medical hypothesis: xenoestrogens as preventable causes of breast cancer.

The article begins with a discussion of the rationale for studying the relationship between residential environments and cardiovascular health. Existing empirical research relating residential environments to cardiovascular outcomes and risk factors is summarized. The research areas discussed include neighborhood socioeconomic characteristics and cardiovascular disease, the effects of residential environments on physical activity, and the effects of residential environments on diet. Other mechanisms through which residential environments may affect cardiovascular health are also briefly noted. Key challenges in investigating the relationship between residential environments and health are discussed. These challenges include characterizing environments (including definition and geographic scale as well as conceptualization and measurement of relavant features), the limitations of observational studies, and the need to evaluate the health impact of interventions or “naturally” occurring changes in local environments. The need for interdisciplinary work is emphasized.

/pdf/residential-environments-and-cardiovascular-risk-2tmi6ugyls.pdf

Residential Environments and Cardiovascular Risk

Since the late 1950s, more than 750 million tons of toxic chemical wastes have been discarded in an estimated 30,000 to 50,000 hazardous waste sites (HWSs). Uncontrolled discarding of chemical wastes creates the potential for risks to human health. Utilizing the National Priorities Listing (NPL) of hazardous waste sites developed by the United States Environmental Protection Agency (EPA), this study identified 593 waste sites in 339 U.S. counties in 49 states with analytical evidence of contaminated ground drinking water providing a sole source water supply. For each identified county, age-adjusted, site-specific cancer mortality rates for 13 major sites for the decade 1970-1979, for white males and females, were extracted from U.S. Cancer Mortality and Trends 1950-1979. Also, HWS and non-HWS counties that showed excess numbers of deaths were enumerated for each cancer selected. Significant associations (p less than .002) between excess deaths and all HWS counties were shown for cancers of the lung, bladder, esophagus, stomach, large intestine, and rectum for white males; and for cancers of the lung, breast, bladder, stomach, large intestine, and rectum for white females when compared to all non-HWS counties. There were no consistent geographical patterns that suggested a broad distribution of gastrointestinal cancers associated with HWSs throughout the United States, although we did identify a cluster of excess gastrointestinal cancers in counties within states located in EPA Region 3 (Delaware, Maryland, Pennsylvania, Virginia, West Virginia).(ABSTRACT TRUNCATED AT 250 WORDS)

Cancer Mortality in U.S. Counties with Hazardous Waste Sites and Ground Water Pollution

Vaccination, illness, and smoking history were compiled for a young adult male population. The relationship of cigarette smoking to hemagglutination inhibition antibody response after exposure to a new antigen was assessed in serum specimens collected from 289 volunteers after the 1968 A2/Hong Kong/68 influenza epidemic. Titers were minimally increased among smokers who were sick compared with those of nonsmokers. Among smokers who remained well, titers were significantly increased, probably because of more frequent subclinical infection. The persistence of hemagglutination inhibition antibody after natural infection or vaccination with A2 antigens was significantly decreased among cigarette smokers, as were titers two weeks after vaccination. Serologic response to vaccination did not significantly differ between smoking groups. Smoking, vaccine history, and morbidity status during an influenza epidemic were significant factors in explaining variations in hemagglutination inhibition antibody titers.

Cigarette smoking and hemagglutination inhibition response to influenza after natural disease and immunization.

Analysis of daily mortality for 422 places in the United States from 1962 to 1966 provided a consistent set of mortality predictors of three classes: annual cycle, day of week, and Christmas holidays; influenza epidemics; and days or spells of extreme cold or heat. Analysis of deaths for New York metropolitan region, with daily SO2 measurements in Manhattan at the Davis Laboratory, showed the pollution measurement contributes significantly to prediction of deaths. Mortality was 1.5% iess than expected on 232 days with SO2 levels below 30μg/cu m and 2% greater than expected on 260 days with SO2 levels above 500μg/cu m, after correcting for the other factors. Coefficient of haze (COHS) does as well as SO2 in predicting death. A parallel analysis in the Philadelphia area showed similar, but weaker, SO2 and COHS effect.

SO2 levels and perturbations in mortality. A study in the New York-New Jersey metropolis.

The incidence of acute respiratory illness in families in Chattanooga, Tennessee was studied in 1972 and 1973 to determine if residents of a formerly high nitrogen dioxide exposure community continued to experience a high incidence of illness after ambient air concentrations of the pollutant had been reduced substantially. Illness data were collected by telephone at 2-wk intervals and illness rates per 100 person weeks of observation were contrasted with air pollution concentrations measured no more than 3.2 km from the home. Data were contrasted by communities designated as high, intermediate, or low pollution exposure. In 1972, higher rates of respiratory illness continued to occur in the designated high pollution area. These were associated with current higher short-term concentrations of nitrogen dioxide even though the long-term mean concentrations of the pollutant were little higher than those in the low pollution area. It was not possible to attribute the excesses in illness to specific pollutants or to specific exposure periods. However, reduction of the illness rate in 1973 associated with a strike at the primary source industry that curtailed nitrogen dioxide pollution in the high exposure community suggested that the short-term exposure may be more important than long-term exposure.

Wilson B. Riggan

Papers

Cancer Mortality in U.S. Counties with Hazardous Waste Sites and Ground Water Pollution

Cigarette smoking and hemagglutination inhibition response to influenza after natural disease and immunization.

SO2 levels and perturbations in mortality. A study in the New York-New Jersey metropolis.

Acute respiratory illness in families exposed to nitrogen dioxide ambient air pollution in Chattanooga, Tennessee.

Trends in the geographic inequality of cardiovascular disease mortality in the United States, 1962-1982.