First off, props to Dr. Isis, who in the discussion of her Cairo haze post referenced the work of L. Calderón-Garcidueñas, which set me off into the literature. What I have initially found was sobering.
Air isn't something we often think about. We take it entirely for granted. We complain about how hot or humid it is, but we usually don't have to think about what in that air might be making us, or our children, sick. Those of us fortunate enough to live in Western, industrialized countries really are well-off in that we don't ever really have to pit our own health against the simple act of breathing. Other areas in the world aren't so fortunate.
Dr. Calderón-Garcidueñas' work focuses on the effects of airborne pollutants and particulate matter on the developing lungs of children in Mexico City, Mexico. But her work is actually relevant to anywhere that the air isn't shiny clean.
By radiograph, her team found that children in Mexico City with lifelong exposure to the polluted air had significantly increased rates of lung hyperinflation when compared to age-matched controls from a much less polluted area (Tuxpam, Ver [I'm guessing this is somewhere else in Mexico?]). Lung hyperinflation by itself in one person doesn't indicate a lot, it just means that there is more air in the small alveoli of the lung so it appears larger on a radiograph. This could mean asthma, emphysema, or even lung cancer, but could also just mean the patient was breathing hard. But when there is such a significant (p=0.0004) between groups it becomes indicative of pollution-induced lung dysfunction.
This is in addition to previous work demonstrating that children in this severly polluted area of Mexico City had altered nasal apparatus such that the mucociliary clearing/filter mechanism wasn't working so well as it should be. This is troubling because the loss of the nasal ciliary filter leads to an even greater dose of reactive gasses or particulate matters getting past it into the lower lungs, thus exacerbating the initial problem.
Referenced experiments in this paper showed even more going on. Particulate matter (PM) less than 5um in aerodynamic diameter was found to disproportionately wind up in the alveolar sacks of the lung while PM greater than 10um was found to locate to the proximal bronchioles. PM doesn't seem to affect lung epithelia directly, but it does activate alveolar macrophages to produce inflammatory cytokines (IL-6 and TNF) that utlimately will attract additional inflammatory infiltrate and further damage lung tissues. On the other hand, reactive gasses were found, in vitro and in animal models, to elicit secretion of IL-6, IL-8 (both inflammatory), and fibronectin (involved in repair if tissue damage) in lung epithelial cells.
Together, these 2 overlapping respsonses indicate the air pollution is driving a repetitive damage-repair cycle in lung tissues. Pollution damages lung tissue and activates the immune system to produce and inflammatory response. So the lung tissue tries to repair itself in an inflammed environment, which can lead to scar-like tissue regeneration. The altered tissue regeneration (as in the loss of the nasal cilia above) can lead to lung tissue more vulnerable to subsequent pollution injury. Over time, this kind of cycle leads to long-term tissue remodeling such as increased constrictive reactivity of existing smooth muscle (a hallmark of acute asthmatic responses), increased smooth muscle metaplasia (chronic asthma), eosinophilia (asthma and allergy reactivity), and even destruction of the walls dividing alveoli (a hallmark of emphysema). And what's saddest about this is that moving animal models of exposure to clean air did not completely reverse the exposure-related pathologies, which means that the lung damage will be a life-long legacy of any children that grew up in it.
So take a deep breath, and be thankful it's mostly clean.
Calderón-Garcidue˜nas, L. (2000). Respiratory tract pathology and cytokine imbalance in clinically healthy children chronically and sequentially exposed to air pollutants Medical Hypotheses, 55 (5), 373-378 DOI: 10.1054/mehy.2000.1070
(P.S. - Whomever came to this blog searching for "burning bronchioles so they won't constrict", please don't. I can think of few worse ways to die than by one literally drowning in necrotic, burnt lung tissue while gasping painfully for whatever air they can still get.)
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