With this caveat in mind, what did Falck et al show? Because of previous studies linking chronic C pneumoniae infection with atherosclerotic heart disease and with a high-risk atherogenic lipid profile (ie, low high-density lipoprotein and high triglyceride levels) that is also suspected to be caused by chronic, low-grade, Gram-negative bacteremia (C pneumoniae is derived from Gram-negative ancestors), Falck et al first sought to associate IgA antibodies with the clinical manifestations of the metabolic syndrome and failed to show an association. This failure does not necessarily contradict the previous findings but does suggest that, taken as a group, not all clinical syndromes that are risk factors for atherosclerosis (ie, the metabolic syndrome) are associated with persistent C pneumoniae infection, as measured by the IgA antibody level. On the other hand, Falck et al did find associations of C pneumoniae IgA antibodies with a heterogeneous group of chronic respiratory syndromes and with objective evidence for respiratory obstruction, as measured by peak expiratory flow rates. The chronic respiratory illnesses included clinical diagnoses of upper respiratory tract disorders, asthma, and chronic bronchitis/emphysema. Again, the issue of nonspecificity arises: is it credible that C pneumoniae could be causally associated with so many different respiratory syndromes, or is this nonspecificity due to confounding by other unmeasured variables? Evidence now exists that the C pneumoniae organism is present in the target tissues of patients with the syndromes associated by Falck et al with the presence of IgA antibodies, as follows: chronic upper respiratory illness2; asthma5–; and chronic bronchitis/emphysema.6–7 Thus, it is worthwhile to consider the possibility that the serologic associations might, as for smoking, actually be causal.