CVDs are the leading cause of hospitalizations and deaths in COPD patients [22, 23], however, it remains elusive on the prevalence of COPD in patients with hypertension in China. Based on the survey from the community-based nationally representative sample, this study provides the first population-based evidence of the prevalence of COPD in patients with hypertension, both with and without adjustment for diagnostic history of cardiovascular risk factors. Our study demonstrated that the prevalence of COPD among the Chinese hypertensive population aged 40 or above was 15.6%, and the prevalence of COPD among residents aged 40 or above nationwide was 13.6% from 2014 to 2015 [18]. Our finding indicates the prevalence of COPD is higher in hypertensive patients, which makes the hypertensive patients the key group for early screening of COPD. Admittedly, studies have shown that there is a close relationship between COPD and CVDs, and they affect each other [3, 4, 14]. COPD can increase the risk of CVDs such as hypertension, coronary heart disease, and stroke. The mechanism is related to airflow limitation that may lead to a certain degree of systemic inflammatory response. On the other hand, CVDs are generally perceived to be the most important comorbidities in COPD, and COPD patients with CVDs have increased difficulty with clinical treatment and worse prognosis.
From the perspective of demographic characteristics, this study showed that the factors positively linked to the prevalence and risk of COPD were old age, low educational level, and male gender among hypertension subjects. Multivariate analysis also showed that male gender, old age, and low educational level were associated with an increased risk of COPD. These findings are consistent with the previous studies on the incidence and death in COPD subjects [18, 24–26]. Moreover, another study identifies smoking, low educational level, physical inactivity, and being underweight as critical modifiable risk factors of COPD-related mortality [23]. Sex-related disparities in COPD patients are mainly caused by the gender difference in smoking, specific occupational exposures, and environmental exposures [19]. Meanwhile, the prevalence difference of COPD in men and women reduces as the smoking prevalence in women increases [27]. One recent study from developed countries has suggested that the prevalence of COPD is now almost equal in men and women, probably reflecting the changing patterns of tobacco smoking [19]. Educational and age disparities may also contribute to increased chronic comorbidities, decreased body function, accumulation of harmful exposures, individual health care awareness, and other factors[24, 26, 27].
Poverty is strongly associated with airflow obstruction (reflected by FEV1/FVC Ratio) at individual and community level across the world. Living in rural areas and poverty are independent risk factors for COPD [28, 29]. This study also indicated a higher prevalence of COPD in hypertension subjects in rural than that in urban areas. It’s perceived to be related to the economic and environmental condition in rural areas, considering that the per capita income of households is much lower than that in urban areas, and that the level of smog exposure of rural residents is higher than that in urban areas caused by coal and biofuels burning for cooking and heating. In 2000, about 60% of rural households in China used biofuels for cooking [30]. No significant difference related to living in rural areas or poverty in COPD prevalence is identified through multivariate analysis, which may be explained by the reduced economic effects due to subject selection with hypertension and tobacco exposure.
Consistent with other similar studies, in the hypertensive population aged 40 or above, our study also revealed that the prevalence of COPD in the underweight group was higher than in the normal weight group, while the prevalence of COPD in the overweight and the obese group was lower than the normal weight group[18, 31, 32]. Zhou Y et al provided comprehensive data about the positive relationship between COPD and low BMI using both cross-sectional and cohort approaches [32]. Furthermore, this conclusion is confirmed by another group to determine the COPD risk factors in Sichuan Province, China [31]. Malnutrition has been thought to be harmful for exercise, muscle, and lung function as well as to increase the risk of exacerbations and mortality, and the expenditure of medical treatment for many years [33–35]. Decreased BMI is the most prominent feature of malnutrition. Low BMI is not only associated with a higher prevalence, but also an increased mortality risk among COPD patients [25]. Nutritional supplement therapy has been recommended as an effective approach for the management of COPD patients [36]. A nationally representative study conducted in China has identified that the relative risks of COPD-related mortality for baseline underweight were 2.66 and 2.60 in men and women, respectively [25], and other studies have estimated that approximately 25–40% of COPD patients are underweight [34]. Because BMI measurement is simple and easy, it is one of the indicators of COPD risk assessment and management. COPD is driven by a diverse range of mechanisms. Our understanding of the biological mechanisms that low BMI contributes to COPD may be explained by systemic inflammation. Considering that COPD is a consumptive disease, underweight and weight loss are common signs of patients [37]. The association between high BMI and low risk of COPD remains to be further verified, which may be the result of confounding factors.
Smoking is the most common risk factor for COPD, which causes respiratory symptoms, harms lung function, declines the FEV1, and increases COPD prevalence and mortality [4, 19, 27, 38]. Moreover, there is a dose-response relationship between the amount of smoking and the degree of airflow limitation [4, 19, 27, 38]. The results of this study also showed that the prevalence of COPD in current smokers and former smokers in Chinese hypertensive patients aged 40 years and above was much higher than that in never smokers. Multivariate analysis also showed that both current and former smoking may increase the risk of COPD in the hypertensive patients, and that the risk of COPD of female who were current smokers was higher than that of male current smokers, suggesting that the risk of COPD of women is more affected by smoking than men, which may be partly explained by the finding that female is more susceptible to the effect of tobacco smoking than male [39]. In 2014, the current smoking rate of people aged 40 or above in China was 31.0%, for men was as high as 57.6%, and for women was 4.0% [40]. One study based on the data of Global Burden of Disease showed that smoking was the most important risk factor for male in each socio-demographic index region [41]. Considering that smoking is a common and modifiable risk factor for hypertension and COPD, reducing tobacco use should be an important measure for COPD prevention and control in patients with hypertension, especially for male patients, which can exert the synergistic effect on reducing the risk of COPD and hypertension.
Given that any factors affecting lung growth during gestation and childhood have the potential for increasing an individual's risk of developing COPD [19]. It is not at all surprising that a higher prevalence of COPD is observed in subjects experiencing tuberculosis and a history of hospitalization for pneumonia/ bronchitis. From the analysis of gender stratification, the history of pulmonary tuberculosis and the history of hospitalization for pneumonia/bronchitis in childhood mainly affected female hypertensive patients, and the reasons remain unclear. Previous studies have confirmed that subjects are more prone to develop COPD with a history of tuberculosis, chronic bronchitis, and any respiratory infection [42–45]. Therefore, we suggest that the promotion of BCG and pneumonia vaccination and physical fitness in children and adolescents should be an important strategy for the prevention and control of COPD.
There is growing evidence that environmental exposures, including biomass fuel exposure and air pollution contribute to COPD development and exacerbation. Indoor air pollution exposure including wood smoke, animal waste and coal fire has been identified as risk factors for many pulmonary diseases, such as acute respiratory infection, lung cancer, asthma, pneumonia, and COPD [19, 46]. Especially, around 30% of deaths due to COPD could be caused by indoor air pollution [47]. Attention has been caught by indoor air pollution including but not limited to traditional cooking stoves and room heating. This study also showed that among patients with hypertension, exposure to smoke from solid fuel burning increased the prevalence of COPD. Mechanistically, airway inflammation, fibrosis and remodeling, increased systemic inflammatory response and oxidative stress, inactivation of alveolar surfactants, reduced bacterial clearance and damaged mucosal cilia clearance are involved in biomass exposure-dependent COPD [48–50]. Our study confirmed that the exposure to indoor air pollution due to solid biomass fuels increased the risk of COPD, while gender-related differences did not exist. Exposure to indoor coal burning for cooking or heating has not been observed to increase the risk of COPD, and further research is needed. Occupational exposure to organic and inorganic dust, chemical agents, and fumes, were associated with an increased risk of COPD, which was a underappreciated risk factor for COPD [51, 52 4, 53]. One study indicated that one in five COPD cases may be attributable to occupational exposures [53]. Our study also confirmed the consistent association between exposure to dust/chemicals in the workplace and increased risk of COPD among men aged 40 and older with hypertension. However, this association was not found in women aged 40 and older with hypertension, which is related to gender differences in occupational exposure [19]. Therefore, the analysis between environmental exposure and the prevalence of COPD in patients with hypertension reveals that preventive strategies should be aimed at reducing the exposure to indoor air pollution and dust/chemicals in the workplace.
The present study has several strengths to be highlighted. Data in the study came from a large and nationally representative sample survey, which followed a strict quality assurance and control protocol to ensure data validity and reliability. However, this study has certain limitations. Firstly, the information, such as childhood hospitalizations for severe lung diseases, history of tuberculosis, family history of lung disease, and indoor and workplace exposures were from self-report, the accuracy of which could not be verified. Secondly, the selected subjects were exclusively residents (6 months or more in the jurisdiction), and non-residents were not included. Therefore, it is uncertain whether these findings can be extrapolated to the non-residents. Thirdly, the exclusion of the subjects with contraindications for lung function test for safety reasons may cause selection bias. Finally, we used data that was collected during 2014-15 and thus a bit older. However, this is the latest available data on COPD collected at the national level.