Public health intervention relies on a science-based evidence or prior vetted knowledge for preventative or control measures for existing or emerging public health challenges. Unfortunately, establishing a conclusive epidemiological evidence for a disease or health event especially chronic conditions may take many years or even decades to achieve convincing dataset. The looming global risk factors to chronic conditions and infectious diseases are consequences of human activities. For instance, air pollution and a variety of genetically modified organism (GMO) crops have been linked to chronic diseases.
In part, the increase in air pollution results from increased use of fossil fuel and the outsourcing/globalization of productions or human activities to regions with unregulated or sub-standard public health regulatory infrastructures or info-structures (Dong, et al., 2012). Some of the outsourced regions especially developing countries do not have adequate, or sufficient infrastructures to regulate and control toxic chemicals or particles. In addition, urbanization and rapid economic developments have drastically increased outdoor pollution and has taken precedence over environmental safety. China and India are clear evidence to this effect. Air pollution in China and India have increased drastically in the past decades (Dong, et al., 2012).
The 12-years retrospective study conducted by Dong et al., (2012) in Shenyang, China, assessed the correlations between outdoor pollutants particular matter <10 um (PM10), sulfur dioxide (SO2), and nitrogen dioxide (NO2) to mortality rate. The data used in the study was dated January 1st 1998 to January 1st of 2009 from 10 communities with approximately 13, 000 cohorts (Dong, et al., 2012). Out of the 12,584 cohorts, 9941 (79%) cohorts completed the study questionnaire (Dong, et al., 2012). The inclusion criteria, ethic committee, and informed consent were implemented in the study. Some of the confounding criteria that were considered and adjusted for in the study were smoking, alcohol consumption, socioeconomic status (education), age, sex, residential area, residential history, lifetime use of household stove or fuel, diet, marital status, occupational history, exercise frequency and medical history for 1998 through 2009 (Dong, et al., 2012).
The data generated from the study showed that PM10 and NO2 (air pollutants) were directly linked to the risk of mortality from respiratory diseases (Dong, et al., 2012). The study was consistent with published findings in developed countries. However, the risks were greater in China than in developed countries such as the US, Europe, and Japan. The increased exposure (air pollutants) risks in Shenyang, China ranges from 27-286% (Dong, et al., 2012). Also, the study indicated that with the SO2 pollutants, there was no significant difference observed (Dong, et al., 2012). However, the observation does not mean that SO2 pollutants do not cause any toxic effect to humans or the environment, but the consensus was that PM10 and NO2 toxicity masked the effects of SO2 in a long-term study (Dong, et al., 2012). In contrast, in a short term study, SO2 pollutants have been demonstrated and linked to acute respiratory effects to human lungs (Dong, et al., 2012). In addition, the study suggested that women are at higher risks than men in developing respiratory disease or higher respiratory mortality rate (Dong, et al., 2012). The risk differences between women and men are because of the inherent differences between men and women Airways from early fetal lung development and throughout the lifespan (Dong, et al., 2012).
In addition, dose-response is detected easily in women, and greater lung particle depositions of 1uM are deposited in women than in men (Dong, et al., 2012). From previous studies, BMI and smoking are directly associated with respiratory mortality. Also, the Dong et al. (2012) study showed that people with normal BMI had higher respiratory mortality than people with 18.5 or 25 or greater BMI, the reason for the discrepancy, was not clear. However, the study confirmed that PM10, SO2, and NO2 increased mortality rate in smokers than in non-smokers (Dong, et al., 2012).
GMO is another increasing area that demands independent epidemiological studies in human. GM crop regulations and approvals rely on the assumption that the principal toxic/allergic component in GMO food product is the protein expression and protein toxicity of the gene of interest (GOI). Thus, GMO products approval processes are based on the protein digestibility and toxicity analysis or pharmacokinetics and pharmacology or the absorption, distribution, metabolism and excretion (ADME). In a sharp contrast, the lapse of scientific possibility that DNA consumption from GM crop (the inserted GOI) can be taken up by the intestinal bacteria to create resistant or mutant strains is not seriously considered (D’agnolo, 2005).
The European Union (EU) regulatory agency denied the approval of Bla gene for the Bt corn (event number 176) during the first approval application process on the ground that Bla DNA extract can be integrated in the intestinal bacteria. However, the “GMO product” was approved by EU in 1996 after other experts asserted that Bla gene posed no significant antibiotic risks (D’agnolo, 2005). Overall, the common allergenic food accounts for more than 90% of food allergies, and over 200 food are characterized as allergens, and 20% of true immune-pathological adverse reaction are food related (D’agnolo, 2005). The epidemiological effects of GMO food products to humans, and its association with chronic/infectious diseases should follow the same or similar study profile as any other known chronic disease risk factors in order to establish a transparent and meaningful scientific evidence on public health issues.
References
D’agnolo, G. (2005). GMO: Human risk assessment. Veterinary Research Communications, 29(Suppl. 2), 7–11. DOI: 10.1007/s11259-005-0003-7
Dong, G., et al., (2012). Long-term exposure to ambient air pollution and respiratory disease mortality in Shenyang China: A 12 year population-based retrospective cohort study. Respiration, 84(5), 360–368. doi: 10.1159/000332930
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