Occupational physical activities contributed to high levels of total activity-related energy expenditure in our study , and we did not find an association of AMI risk with the agricultural or manual labor job patterns. Our study has several limitations that must be kept in mind in interpreting our study findings. Our study is a case-control study and, thus, the temporal relationship between physical activity and AMI risk is unclear. As in all observational studies, we cannot establish causal associations. Self-reported physical activity measurements contain large measurement error, which may lead to underestimate the effect of physical activity on AMI risk. Recall bias is an issue in case-control studies. If controls are more likely to under-report daily physical activities than cases, the results could be biased towards the null hypothesis; if controls, due to social desirability, overestimate their physical activities while cases do not, then the effects of physical activity could be overestimated. However, our results on total activity-related energy expenditure are consistent with those from previous studies. Thus, recall bias is less likely to play a role in our study. Another potential limitation is that cases only included survivors of a first AMI. We cannot exclude residual confounding in our estimates. For example, occupation stress, a potential confounder, was not accounted for in our study because the information was not available. Our results may not be generalizable to other populations, since physical activity patterns are likely to vary according to many factors such as population level economic development, individual level socioeconomic status, the built environment, and distribution of leisure and occupational activities.Asthma morbidity and mortality have steadily increased since the mid-1970s , possibly reaching a plateau recently,greenhouse grow racks but the causes of this rise are largely unknown. The rise in allergic rhinitis may have begun after the inception of the industrial revolution .
The possibility of a linkage between the rise in asthma and in allergic rhinitis is supported by the consensus that the two diseases share certain genetic and environmental determinants . During the time that asthma increased, regulated ambient criteria air pollutants generally decreased in the United States. Because the two time trends are not positively related, arguably the rise in asthma could not be due to exposure to ambient air pollutants. This argument is not valid because correlations between time series are subject to ecologic fallacy. This biased interpretation can occur when associations at an aggregate level do not represent associations on an individual level because of unrelated causal factors that independently drive one or both of the aggregate trends. The bias may be amplified if trends in synergistic or antagonistic factors are ignored. For example, a lifestyle risk factor or other environmental exposure may have increased over the same period, and that factor could have positively interacted with effects of the regulated air pollutants. Many factors associated with Western industrial life other than environmental pollution have been identified as potential causes for the asthma epidemic, including allergens from indoor carpeting and pets coupled with increases in indoor residence time and in building tightness, early antibiotic use that prevents differentiation toward T-helper type 1 lymphocytes , declining physical fitness, and diet . Acute asthma morbidity has been associated with specific regulated air pollutants in aggregate time series and in individual-level repeated measures studies [reviewed by Bascom et al.. The risk of asthma onset or chronic effects on asthma from ambient air pollution exposure has been less clearly identified in epidemiologic studies, although few studies are prospective cohort designs . A cohort study of nonsmoking adult Seventh Day Adventists in California followed 10 or more years found associations between the development of asthma and outdoor concentrations of total suspended particulates , total suspended sulfate , and ozone . The association for O3 was found in males but not in females, possibly because males in that study spent significantly more time outdoors than females .
Three cohort studies looked at lung function growth in children and found significant reductions in growth of forced expiratory volume in 1 sec and forced vital capacity in relation to increasing levels of ambient air pollutants, including nitrogen dioxide , particulate matter < 10 and < 2.5 µm in aerodynamic diameter , O3, sulfur dioxide , and black smoke . Diminished lung function growth is one of the possible adverse outcomes of poorly controlled asthma . Epidemiologic studies of asthma and ambient air pollution have focused primarily on five of six principal criteria air pollutants for which the U.S. Environmental Protection Agency has established so-called National Ambient Air Quality Standards : O3, PM, carbon monoxide , NO2, and SO2. Studies in Europe have also used black smoke, which can represent sources of complex exposures such as DE that have a high elemental carbon content. The causal components in the epidemiologic studies have not been clearly identified, partly because the measurements have included only those major pollutant types that a) co-vary with other photochemically produced pollutants ; b) involve complex particle mixtures that vary by space and time ; or c) are correlated with other cogenerated primary pollutants . The availability of government monitoring data and the regulatory focus partly explains the lack of epidemiologic data concerning other potentially important exposures such as air toxics. Experimental research on the respiratory effects of air toxics is largely limited to animal models or in vitro studies. This is not surprising given that many air toxics have potentially serious adverse consequences such as carcinogenic, reproductive, or neurological effects. The occupational literature, on the other hand, has data on high exposures that may be less frequently encountered in nonoccupational settings. Given the lack of information on the causal role in asthma of a large number of potentially important air pollutants, it is important at this stage to identify information that future research can build upon. This article provides a review of the literature relevant to this issue. A major objective is to establish conceptual linkages concerning potential adverse respiratory effects of air toxics between different foci of research, including occupational, indoor, and community air pollution research.
Air toxics can be defined as having three characteristics: a) they have the potential to cause serious adverse health effects in the general population or to organisms in the environment as a result of airborne exposures; b) they are released from anthropogenic sources; and c) they include 189 hazardous air pollutants listed in section 112.b.1 of the Clean Air Act of 1990. It is conceivable that personal exposures to some air toxics may have increased over the last several decades and been partly responsible for the increase in asthma. Most notably, the U.S. Department of Transportation reports that the number of ton-miles carried by intercity trucks has steadily increased from 285 billion ton-miles in 1960 to 1,027 billion ton-miles in 1998, and the amount of diesel fuel consumed also increased in parallel . Over the same period, the total motor vehicle fuel consumption nearly tripled . Traffic density has also increased in many cities along with stagnation in fuel economy since the early 1980s . As a result, it is expected that concentrations of traffic-related pollutants will have increased in certain urban micro-environments. It is relevant that minority groups most at risk for poor asthma management and subsequent disease progression are more likely to live in areas failing to meet the NAAQS. This includes 80% of Hispanics and 65% of Blacks compared with 57% of Whites in the United States . Asthma has been defined as having three phenotypic characteristics: intermittent and reversible airway obstruction; increased airway responsiveness to contractile stimuli; and airway inflammation. Pulmonary inflammation is a hallmark of asthma and is directly related to asthma severity as a function of acute and chronic airflow obstruction. One potential mechanism of action for air toxics is through enhancement of airway inflammation. Inflammation in asthma, however,greenhouse growing rack has diverse pathways, mirroring the complexity of the disease. Three general mechanisms of inflammation in asthma include immunoglobulin E -mediated, neurogenic, and irritant induced. The principal inflammatory mechanism in asthma is an IgE-mediated reaction whereby an antigen cross-links with an IgE antibody specific to that antigen on the surface of mast cells and other immune cells. Commonly recognized antigens that induce acute exacerbations of asthma are high molecular weight allergens such as pollen, fungal and animal proteins. Low molecular weight agents involved in IgE-mediated reactions, including certain air toxics, act as haptens. Haptens must first react with endogenous or exogenous proteins to form a complete antigen . IgE-mediated mechanisms are key in early-phase asthmatic reactions . Other processes follow over several hours and involve the recruitment of eosinophils, CD4+T cells, neutrophils, basophils, and macrophages, and the release of proinflammatory mediators and cytokines. T-cell activation leads to the release of Thelper cell type 2 -like cytokines, which may be involved in a more prolonged chronic phase of inflammatory response over days .
The involvement of TH2 cells is important because a key pathway to the development of the asthma phenotype is believed to be the early differentiation of T-helper lymphocytes into TH2 rather than TH1 cells, although this is still controversial . TH1 cells participate in delayed-type hypersensitivity reactions. TH2 cells promote antibody immune responses, and because they secrete eosinophil-active cytokines and enhance IgE synthesis, they are implicated in the genesis of allergic inflammation.TH0 cells then differentiate into TH1- or TH2-type lymphocytes after repetitive antigen stimulation . Interleukin -4 shifts the differentiation from TH1 to TH2. The balance toward TH2 cells may be tipped by early environmental influences, including exposure to air pollutants , coupled with genetic susceptibilities. This is presumed to be key in the development of asthma. Neurogenic inflammation involves a spread of the inflammatory response via the release of neurotransmitters or activation of afferent nerves by the action of inflammatory mediators . Inflammatory mediators can trigger the activation of nonadrenergic, noncholinergic nerves to release tachykinins. A cascade of bronchoconstrictive reflexes and of inflammatory events can follow. Reactive airways dysfunction syndrome is a primary example of a type of asthma where toxic irritant-induced inflammation is a key mechanism. RADS has been identified in occupational settings and is defined as an irritant-induced nonimmunologic asthma with no latency period. RADS is nonimmunologic in the sense that bronchial epithelial injury is the primary causal event and typical phases of the immune response are absent, namely, sensitization, latent period, episode of elicitation of an immune response to antigen, and repetitive elicitation . RADS is an example of an inflammatory mechanism of air toxics, but it is rare and its relevance to nonoccupational asthma is unclear. There is hypothesized to be a feedback loop between inflammatory processes and neuronal processes that trigger inflammation . The inflammatory processes can be either immune mediated or triggered by irritant-induced airway injury. For RADS , and to some extent oxidant pollutants such as O3 , the initiation of bronchial epithelial injury could initiate the release of inflammatory mediators. This inflammation could then trigger neurogenic inflammation. Chemical irritants may also act as neuronal triggers directly . Irritant-induced induction of tachykinin release could serve to enhance ongoing inflammation in the asthmatic lung caused by known immune triggers. Examples consistent with this hypothetical mechanism include the putative interaction between ozone and pollen in asthma exacerbations , and the finding in subjects with mild asthma that airway responsiveness to inhaled allergen increases after ozone challenge . Airborne irritants could also indirectly enhance neuroinflammation by inhibition of neutral endopeptidase . NEP degrades tachykinins and its levels are decreased following exposure to oxidants , cigarette smoke , and an agent responsible for a form of occupational asthma, toluene diisocyanate . PAHs are found in relatively high concentrations in automobile and DE, along with other potentially important chemicals including nitroaromatics, aldehydes, alcohols, ketones, quinones, phenols, and other organic compounds, as well as volatile co-pollutants— oxides of nitrogen and of sulfur, CO, and numerous VOCs such as formaldehyde, benzene, and 1,3-butadiene. Diesel exhaust particles have a submicrometer elemental carbon core coated with organic compounds , nitrites, sulfites, and trace metals. The most common type of PAH compound in DEPs includes the phenanthrenes, followed by fluorenes, fluoranthrenes, naphthalenes, and pyrenes . However, PAHs are semivolatile, and so much of the PAHs emitted from motor vehicles is not particle bound. Selected indoor home concentrations of various semivolatile PAH compounds for 33 homes in Californiaand Ohio ranged from 9.2 to 210 ng/m3 for phenanthrene, 0.29 to 1100 ng/m3 for quinoline, 2.40 to 37.4 ng/m3 for fluoranthrene, and 0.00 to 4.13 ng/m3 for benzo[a]pyrene .