There has been little study of ethnic differences in the impact of asthma on lung function. The Harvard Six-Cities Study found no differences between blacks and whites in the effect of asthma or wheeze on the levels of FEV1
and MMEF in the preadolescent and adolescent years (41
). To our knowledge, differences in the impact of asthma among Hispanics and non-Hispanic whites have not been reported previously. We found larger asthma-associated deficits in Hispanic than in non-Hispanic white children, especially among girls. Hispanic girls had significantly larger deficits in flows (FEV1
, MMEF, and PEF) than non-Hispanic girls, differences that were limited to those diagnosed after 4 years of age. A similar pattern of effects was observed in boys, although the differences in flows were significant only for FEV1
(in a sensitivity analysis restricted to children with health insurance). There was little, if any, effect of asthma on lung function in non-Hispanic children with asthma diagnosed after age 4 years, regardless of sex.
We evaluated possible reasons for these differences based on our hypothesis that they could be explained by social factors, SHS exposure, and housing characteristics, but information available did not explain the ethnic differences in the impact of asthma on lung function. Hispanic children were less likely to have insurance (), and this might have explained the observed differences in flows, especially in girls, if lack of access to care resulted in delayed diagnosis of early onset asthma (which was associated with larger deficits in both ethnic groups) or suboptimal treatment. However, one might expect this explanation to have resulted in attenuated effects after statistical adjustment for health insurance or restriction to children with insurance, which was not the case. Lack of access to care might also be reflected in a lower proportion of symptomatic Hispanic children being diagnosed with asthma early in life, but we found little evidence for this because most children were diagnosed after 4 years of age, regardless of sex or ethnicity. Hispanic children with wheeze in the previous year were slightly more likely to have a doctor diagnosis of asthma at study entry (54%) than were non-Hispanic children (50%). Therefore, delayed diagnosis seems an unlikely explanation for the ethnic differences in flows in girls. In an additional sensitivity analysis, the larger deficits in flows in Hispanic girls were generally limited to those who had late-onset asthma and medication (inhaler) use (data not shown). Information on type of inhaler (controller or rescue medication) was not available. It is possible that the differences in lung function were explained by treatment with controller medications, if lack of insurance resulted in fewer Hispanic children being treated. However, although some studies have suggested that inhaled corticosteroids in older children and adults improved lung flow rates (49
), several randomized trials in children found no long-term beneficial effects of controller medication on lung function (50
). Other investigators have found that lung function was lower in children of lower SES (52
). Hispanic children's lower prevalence of health insurance coverage and lower parental educational attainment (), compared with non-Hispanic children, are markers for lower SES, but adjustment for parental education also did not explain the pattern of lung function differences.
Indoor allergen exposure associated with poor housing conditions and in utero
and SHS exposure may modulate the severity of asthma and the impact on lung function (10
). However, adjustment for mold or mildew and for cockroaches in the home did not alter the pattern of ethnic-specific effects of asthma on lung function. Tobacco smoke exposure was uncommon among Hispanics compared with rates in non-Hispanics (), and adjustment for in utero
, SHS exposure and for personal smoking in the year before each lung function test also did not explain the ethnic differences.
The impact of asthma on FVC in boys was marginally statistically different from the effect in non-Hispanics. However, this difference was partly caused by the larger FVC (albeit not significantly so) in non-Hispanic children with asthma compared with non-Hispanic children without asthma ( and ). The difference between Hispanics and non-Hispanics also was reduced and was no longer significant in the sensitivity analysis excluding African Americans and Asians from the analysis. Thus, this pattern of ethnic difference may have been caused by chance.
Other environmental exposures and cultural characteristics, especially dietary differences, and genetic variation merit further investigation as possible causes for the observed ethnic differences. Genetic variation has been shown to modulate the effect of asthma on lung function among Hispanics (53
), and we have previously shown that genetic variation in susceptibility to tobacco smoke may affect lung function deficits among children with asthma (12
). The use of race and ethnicity in studies such as ours is controversial (54
); Hispanics may not even be aware of their precise racial background and may report ancestry based on physical appearance and family national origin (37
). Populations similar to our southern California population, which is primarily of Mexican origin with a smaller proportion from Central America, have been reported to have on average 52% Native American and 45% European ancestry (37
). The ethnic pattern of effects of asthma was not substantially affected in the sensitivity analysis excluding those reporting African American or Asian ancestry. Our results could not be generalized to Puerto Ricans, who have different racial ancestry, higher prevalence of lifetime physician-diagnosed asthma and active physician-diagnosed asthma, earlier onset of asthma, and lower lung volume than Mexicans (36
), or to other Hispanic groups. Nevertheless, distinguishing genetic from poorly characterized environmental causes that are correlated with genetic ancestry requires consideration of ethnicity (55
Our results should be interpreted in light of some limitations to the study. First, the lack of adequate sample size from other racial and ethnic groups precluded their evaluation in this study. Second, variation in loss to follow-up based on characteristics, such as SHS exposure at study entry (see
Table E1 in the online supplement), could limit the generalizability of our results to those who were lost to follow-up. However, controlling for these factors did not explain our results, so bias caused by loss to follow-up seems unlikely to explain the results. Third, asthma is a complex chronic inflammatory disease for which there is no universally recognized definition. Case ascertainment was done by parental report of physician-diagnosed asthma without clinical examination, which is widely used in epidemiologic studies (57
), is reproducible (58
), and is a valid measure of what physicians actually report to patients (60
). The rates of asthma were high, partly because we included both lifetime cases at study entry () and cases reported at yearly follow-up (Table E1). This design may also help explain why most cases were diagnosed after age 4 years, although it is commonly believed that most asthma originates in earlier childhood (2
). Because we did not follow the cohort from birth, we cannot directly determine whether a new diagnosis during follow-up truly represented a late-onset incident case or was a second occurrence of asthma that first occurred during infancy but was not reported by a parent on the baseline questionnaire. Rates of new onset asthma in this cohort, which we have previously reported (62
), are high compared with reported incidence rates of childhood asthma in earlier decades (64
). However, the rates in this cohort reflect the increasing rates of prevalence of asthma and of incidence measured more recently in similar study designs around the world (67
). Although differences in design preclude comparison with rates in many other studies, reported age of onset has been validated and has provided reliable estimates in questionnaire-based longitudinal studies (76
). We also found that girls were more likely to develop asthma during later childhood than boys, results consistent with previous studies (77
). Although misclassification of asthma might affect the observed impact on lung function, this is an unlikely explanation for the pattern of observed results unless misclassification was differential with respect to sex and ethnicity.
Finally, deficits in flows are an indicator of asthma severity (81
), but acutely these deficits may reflect reversible bronchospasm and chronically they may reflect remodeling and fixed obstructive defects (8
). We had limited ability to distinguish these two interpretations of the data, for example by evaluating the individual response to bronchodilators. However, the ethnic differences in asthma-associated lung function deficits did not change after adjustment for use of an inhaler at the time of PF testing or for severe wheeze (as defined in the online supplement), both of which may have been markers for disease exacerbation. These sensitivity analyses suggest that the observed lung function deficits were chronic.
A major strength of this study is the large sample size and yearly assessment of asthma and lung function from childhood through adolescence, which made it possible to identify the larger effects of asthma on lung function among Hispanics, especially on indicators of obstruction (MMEF and FEF75
) in girls diagnosed after age 4 years. Although the ethnic differences in mean flow rates were small, large differences were observed in the proportion of children with late-onset asthma with abnormal FEV1
and MMEF (each with 14.8% who were abnormal in Hispanic girls with asthma, compared with 5.1% abnormal in non-Hispanic white girls with asthma). These differences were statistically significant (interaction P
value = 0.06 for ethnic differences), despite limited power caused by relatively small sample size in these subgroups. The largest deficits in flows were associated with diagnosis at early age and did not vary between ethnic groups, results that were consistent with an earlier analysis of a sample of this cohort with shorter follow-up (38
) and with other studies (82
). Further investigation is warranted to determine the implications of these ethnic differences for lung function and associated cardiorespiratory disease, including mortality, in later adult life, and to identify potentially preventable causes (84
). Ethnic differences in dietary and genetic characteristics, for example, might explain the observed differences.