The Journal of Association of Chest Physicians

: 2019  |  Volume : 7  |  Issue : 1  |  Page : 1--9

Respiratory Health Hazards in Women

Kanchan Srivastava1, Apoorva Narain1, Jyoti Bajpai1, Surya Kant2,  
1 Department of Respiratory Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Respiratory Medicine, King George’s Medical University, Lucknow, Uttar Pradesh, India

Correspondence Address:
Surya Kant
Department of Respiratory Medicine, King George’s Medical University, Lucknow 226003


Respiratory tract diseases are public health problems, and these diseases affect the air passages, including the nasal passages, the bronchi, and the lungs. They range from acute infections, such as pneumonia and bronchitis, to chronic conditions such as asthma and chronic obstructive pulmonary disease. The prevalence of chronic respiratory morbidity among females is significantly higher compared to the general population of the country. It is a conditions affecting the organs and tissues that make gas exchange possible and includes conditions of the upper respiratory tract, trachea, bronchi, bronchioles, alveoli, pleura and pleural cavity, the nerves, and muscles of breathing. Females had respiratory illness were also higher among the users of tobacco and alcohol. Respiratory diseases range from mild and self-limiting, such as the common cold, to life-threatening entities such as bacterial pneumonia, acute asthma, and lung cancer. When women must cope with respiratory disease in the face of significant psychological, social, or cultural challenges, such as depression, economic burdens, competing family responsibilities, or disease stigma, the risk of nonadherence may increase. Women response with drugs is a big issue, because women of child-bearing age were excluded from participating in clinical studies, and information regarding gender-dependent responses to drugs in general and to respiratory drugs specifically has been lacking.

How to cite this article:
Srivastava K, Narain A, Bajpai J, Kant S. Respiratory Health Hazards in Women.J Assoc Chest Physicians 2019;7:1-9

How to cite this URL:
Srivastava K, Narain A, Bajpai J, Kant S. Respiratory Health Hazards in Women. J Assoc Chest Physicians [serial online] 2019 [cited 2019 Feb 22 ];7:1-9
Available from:

Full Text


Respiratory tract diseases are diseases that affect the air passages, including the nasal passages, the bronchi, and the lungs. It is a term that covers pathological conditions affecting the organs and tissues that make gas exchange possible in higher organisms. Respiratory diseases range from mild and self-limiting, such as the common cold, to life-threatening entities such as bacterial pneumonia, pulmonary embolism, acute asthma, and lung cancer.[1],[2],[3] The human respiratory system is a series of organ having two different types of respiration: cellular and physiological, the latter of which concerns the process of breathing and the respiratory system. At the same time, carbon dioxide (CO2) is transmitted from the blood capillaries into the alveoli and then expelled through the bronchi and the upper respiratory tract. The inner surface of the lungs where the exchange of gases takes place is very large, due to the structure of the air sacs of the alveoli. For humans and other oxygen-breathing vertebrates, the process of respiration takes place within the lungs, driven by a series of mechanics called inhalation and exhalation. These are the biological mechanisms that make up breathing. The entire process uses the nasal cavity, the mouth, the larynx, the trachea, and the bronchial tubes of the lungs as well. We consider the respiratory illnesses such as asthma, chronic obstructive pulmonary disease (COPD), obstructive sleep disorder, lung cancer, interstitial lung diseases (ILD), and tuberculosis (TB) are caused by smoking and biomass fuel.

Respiratory disease is a common and significant cause of illness and death around the world. Approximately 1 billion “common colds” occur each year. Approximately one in seven individuals are affected by some form of chronic lung disease, most commonly COPD, chronic bronchitis, and emphysema.[3],[4],[5],[6] Respiratory tract diseases affect the air passages, including the nasal passages, the bronchi, and the lungs. They range from acute infections, such as pneumonia and bronchitis, to chronic conditions such as asthma and COPD.[3],[4],[7],[8],[9],[10] Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause (etiology) of the disease.[11],[12],[13],[14],[15] Women may have differences in symptom expression, disease progression, and comorbidity patterns (e.g., depression and osteoporosis).

 Gender Differences in Airway Anatomy

During fetal development, maturation appears to be more advanced in female than male lungs in terms of both fetal breathing and surfactant phospholipids profile. Although female lungs are smaller than their male counterparts, they exhibit higher flow rates during the whole lifespan. In fact, the ratio of forced expiratory volume in 1 s to forced vital capacity is higher in girls and women than in boys and men.[14] Because flow rates seem to be strongly influenced by airway length, the larger lungs of males operate in unfavorable conditions, as their airways are both longer and narrower than those of smaller female lungs. This effect is more prominent in the growing lung, because, at variance with females, in males, the airways grow at slower rates than parenchyma.[16]

Gender differences in the lung physiological behavior are less striking in the adult lung, but it is influenced by biological as well as sociocultural determinants across the human lifespan. Dimensional (including structure/function relationships), immunological, and hormonal factors (all gender based) interact to different degrees and directions with environmental exposures often differently experienced by girls and women compared with boys and men.[16]

Diseases and conditions of the respiratory system fall into two categories: viral infections such as influenza, bacterial pneumonia, and the new enterovirus respiratory virus that has been diagnosed in children and chronic diseases, such as asthma and COPD.[17],[18] Clinical characteristics of lung diseases are airflow obstruction, shortness of breath (dyspnea), damaged and enlarged lungs (emphysema), and respiratory failure.

 Diagnosing and Treating Respiratory Ailments

Common diagnostic tools for diagnosing respiratory disease include chest X-rays and pulmonary function test, measures how well the lungs take in and release air, and how well they circulate oxygen. Bronchoscopy is performed by inserting a tube with a light and camera into the airways—the trachea and the bronchial tubes. A similar procedure is a thoracoscopy, in which an optical device can be use to examine the surfaces of the lungs.

 Respiratory Illness


According to the Global Initiative for Asthma, it can be defined as “Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation.” It is a major noncommunicable disease and serious global health problem affecting all age groups, with global prevalence ranging from 1% to 21% in adults and 1.56% in females, experiencing severe wheezing episodes within a year.[19],[20],[21] Although some countries have seen a decline in asthma-related hospitalizations and deaths, the global burden for patients from exacerbations and day-to-day symptoms has increased by almost 30% in the past 20 years. It is a complex disease resulting from the interaction among genetic susceptibility, host defense, and environmental factors. Gender as a congenital factor in asthma has received little attention. Asthma is one of the most common chronic diseases affecting young adults. There is increasing recognition of its impact upon working-age adults, the importance of adult-onset asthma, and the contribution of undiagnosed asthma to respiratory symptoms.[17],[22],[23] The pattern of asthma increasing in girls after puberty is based in part on the influence of sex hormones on its inflammatory pathophysiology. Asthma is 20% more frequent in women than men over the age of 35. Hormonal changes may affect asthma during pregnancy and at specific times during the menstrual cycle.[23] Women may also have gender-related increased exposure to household, occupational, solid biomass fuels, fragrance, and cosmetic-related chemical triggers, but also psychological ones. Depression and obesity may contribute to increased asthma symptoms or severity.[24],[25]

Symptoms may occur several times in a day or week in affected individuals. Recurrent asthma symptoms frequently cause sleeplessness, daytime fatigue, reduced activity levels, and work absenteeism. Asthma control often changes during pregnancy; in approximately one-third of women, asthma symptoms worsen; in one-third, they improve; and in the remaining one-third, they remain unchanged.[15] Exacerbations and poor symptoms control are associated with worse outcomes for both the baby (preterm delivery, low birth weight, increased perinatal mortality) and the mother both.[17],[23],[24],[25],[26]

The fundamental causes are not completely understood. The strongest risk factors for developing asthma are a combination of genetic predisposition with environmental exposure to inhaled substances and particles that may provoke allergic reactions or irritate the airways, such as indoor and outdoor allergens (house dust, mites in bedding, carpets and stuffed furniture, pollution, pet dander, pollens, and moulds), tobacco smoke, chemical irritants at work place, and air pollution. Other triggers can include cold air, extreme emotional arousal (anger or fear), and physical exercise. Urbanization has been associated with an increase in asthma. Although asthma cannot be cured, appropriate management and medication is the only way to control asthma and enable people to enjoy a good quality of life. There is more consistent evidence that air pollution and environmental tobacco smoke trigger asthma in sensitized individuals. International variations in the prevalence of asthma, together with recent increases in many countries, have focused attention on the role of air pollution.


COPD is a lung ailment that is characterized by a persistent blockage of airflow from the lungs. It is an underdiagnosed, life-threatening lung disease that interferes with normal breathing and is not fully reversible. The more familiar terms of chronic bronchitis and emphysema are now included within the COPD diagnosis. COPD is the intersection of three related conditions—chronic bronchitis, chronic asthma, and emphysema, and is a progressive disease that makes it increasingly difficult for sufferers to breathe.[27],[28],[29]

The worldwide prevalence of COPD is growing faster among women than men in many countries. The overall prevalence of COPD is 4.36%, but among males and females were 5.32% and 3.41%, respectively.[30],[31] The prevalence of chronic bronchitis is also greater in women, where women smoke and found to be increasing with an increase in age. COPD-related hospitalization and mortality rates are higher among women, since 2000, more women than men die each year of COPD. The latest evidence shows that women are more likely than men to develop the bronchitic COPD phenotype rather than the emphysematous one, for reasons that still remain unclear.[34] COPD may have more rapid progression in women, with dyspnea and less activity tolerance for the same level of lung function compared to men, resulting in lower quality of life for women with COPD.[32],[33]

The literature also suggests that females are more susceptible to the unfavorable effects of smoking or biomass fuel exposure having more frequent and severe airway hyperresponsiveness than males. In developed countries, smoking is responsible for over 80% of cases of inflammation of the lining of the bronchial tubes (chronic bronchitis), for most cases of over inflation of the air sacs in the lungs (emphysema), progressive, and incompletely reversible airflow obstruction (COPD).[34],[35] However, these diseases occur in regions where smoking is infrequent.

Previous studies had estimated that about 15% of COPD cases are attributable to workplace exposures. One of the main questions that leaves open to future research is whether the observed effects are modified by smoking, because tobacco smoking is the primary risk factor for COPD. Other remaining questions are related to specific risks with respect to particular occupations, activities, and noxious agents.[33],[36] Patients with chronic lung disease have been reported in communities heavily exposed to indoor biomass smoke pollution.[37] A clinical diagnosis of COPD should be considered in any patient: breathlessness/shortness of breath (dyspnea; “need for air”), chronic cough, localized destruction and infection of the lung (local lung fibrosis and bronchiectasis), abnormal sputum (a mix of saliva and mucus in the airway), and history of exposure to risk factors for the disease.

The primary cause of COPD is tobacco smoke (including second-hand or passive exposure), indoor and outdoor air pollution (such as solid fuel used for cooking and heating), occupational dusts and chemicals (vapors, irritants, and fumes), Frequent lower respiratory infections during childhood.

Spirometry is required after diagnosis. It measures how much air a person can inhale/exhale and how fast air can move into and out of the lungs. It is frequently diagnosed in people aged 40 or older due to its slow development. Comorbidities are cardiovascular diseases, osteoporosis, depression, anxiety, skeletal muscle dysfunction, metabolic syndrome, and lung cancer. COPD is manageable and preventable. Once COPD has been diagnosed, effective management should be based on an individualized assessment of current symptoms and future risks:Reduce symptomsRelieve symptoms

Nonpharmacological treatments are smoking cessation, physical activity, flu and pneumococcal vaccination, and pulmonary rehabilitation.


Presently, tobacco use is the single largest and most preventable cause of premature adult death throughout the world, and it has been known for decades. In many countries, women’s smoking rates are increasing, especially in young women.[4],[5] Smoking can be considered in three classes: current smokers (smoking cigarettes, beedis, or hookah daily), ex-smokers (who had smoked daily and given up), nonsmokers (person who had never smoked), and passive smokers [involuntary inhalation of tobacco smoke (as from another’s cigarette), especially by a nonsmoker]. Women have experienced a rapid increase in COPD and lung cancer mortality over the last 2 decades, reflecting past smoking behavior.[38] In the developing world, smoking is linked with an affluent lifestyle, powerful messages of glamour, independence, mood control, and many more, especially young women, resulting in an increased prevalence of smoking among women. Women are clearly not immune to tobacco-related diseases. Smoking cessation is the most significant intervention to slow the rate of lung function decline.[39],[40]

Biomass fuel

Biomass fuel is any material derived from plants or animals which is deliberately burnt by humans. Wood is the most common example, but the use of wood, animal dung, and crop residues is also widespread. China, South Africa, and some other countries also use coal extensively for domestic needs.[41],[42],[43] Almost 3 billion people worldwide use biomass and coal as their main source of energy for cooking, heating, and other household needs. In these communities, indoor air pollution is responsible for COPD risk than smoking or outdoor air pollution. Biomass fuels used by women for cooking account for the high prevalence of COPD among nonsmoking women.[32],[33] Indoor air pollution resulting from the burning of wood and other biomass fuels is estimated to kill women each year. These materials are typically burnt in simple stoves with very incomplete combustion.[42],[43],[44] Consequently, women and young children are exposed to high levels of indoor air pollution for 3 to 7 h daily over many years. During winter in cold and mountainous areas, exposure may occur over a substantial portion of each 24-h period. Among all, animal dung, on the lowest rung of the ladder, is succeeded by crop residues, wood, charcoal, kerosene, gas, and electricity. Many of the substances in biomass smoke can damage human health. The most important are particles, carbon monoxide, nitrous oxides, sulfur oxides (principally from coal), formaldehyde, and polycyclic organic matter, including carcinogens such as benzo[a]pyrene.[45] Substantial deposition of carbon in the lung (anthracosis) occurred consistently in patients exposed to biomass. Particles with diameters below 10 μm (PM10) can penetrate deeply into the lungs and appear to have the greatest potential for damaging health.[46],[47]

A health effect is determined by the time people spend breathing polluted air, that is, the exposure level. Because of their customary involvement in cooking, women’s exposure is much higher than men’s. Young children are often carried on their mothers’ backs while cooking is in progress and therefore spend many hours breathing smoke.[11],[48]

Obstructive sleep apnea syndrome (OSAS)

OSAS syndrome is a clinical disorder marked by frequent pauses in breathing during sleep usually accompanied by loud snoring. These pauses cut off the oxygen supply to body for a few seconds and halt the removal of carbon dioxide. As a result of this, brain briefly wakes up, reopens the airways, and restarts breathing. This can occur many times during the night and makes proper sleep impossible. This break sleep cycle and can leave tired during the day, difficulty in concentrating or headaches, and morning confusion, forgetfulness, depression, or irritability. People with the condition actually stop breathing up to 400 times throughout the night. These pauses last 10 to 30 s, usually followed by a snort when breathing starts again.[49] OSAS is more common in men than women, and biological differences are important in anatomy variations, obesity patterns, and breathing control. Given equal body mass index (BMI) and age, women have more frequent sleep interruptions with a greater number of obstructive sleep apnea (OSA) episodes in the rapid eye movement phase.[49]

Nocturnal symptoms may include usually loud snoring (bothersome to others), waking up suddenly, restlessness during sleep, and nocturia.[50],[51] OSA and OSAS are subsets of sleep-disordered breathing. Snoring can be a symptom of the sleep disorder, but there’s a big difference between the two.

Community-based epidemiological studies from India have shown that the prevalence of OSAS is 1% to 2% in females.[50] There is no considerable variation in the prevalence of OSAS compared to rest of the world where it is 4% in males and 2% in females. The data combined indicate that menopause is a significant risk factor for sleep apnea in women and that hormone replacement appears to be associated with reduced risk.[13],[52],[53] OSA increases mortality either due to apnea, increased risk of vehicular accidents, associated comorbidities, psychiatric disorders such as depression, bipolar disorder, delirium, and anxiety.

Risk factors that are linked by strong published evidence include obesity, increased neck circumference, older age, pregnancy, smoking, alcohol use, polycystic syndrome, postmenopausal state, genetic predisposition, and familial aggregation. Comorbidities may be diabetes mellitus, hypertension, stroke, and coronary artery disease.

In general, diagnosis can be made by physical examination, aside from the presence of obesity (BMI: >30 kg/m2), an enlarged neck circumference [men >43 cm (17 in), women >37 cm (15 in)], and hypertension. Polysomnography (an overnight sleep study) is required to diagnose OSA. Air flow, blood oxygen level, breathing patterns, eye movements, heart rate, and muscle activity monitoring are also required.

The possible options as a treatment are included such as nasal sprays, continuous positive airway pressure machine (a device that wear over nose or mouth, or both), weight loss, and avoid alcohol and sleeping pills, which make the airway more likely to collapse during sleep and lengthen the times to not breathing properly. Other types of positive airway pressure devices, including the Bilevel Positive Airway Pressure (BiPAP/BPAP), which has two levels of air flow and oral or dental appliances or oral “mandibular advancement” devices that prevent the tongue from blocking the throat or advance the lower jaw forward can be made. These devices help keep the airway open during sleep and provide continuous air through the nose or mouth. The air pressure is just enough to keep the upper airway tissues from collapsing during sleep. Upper airway stimulator, somnoplasty, uvulopalatopharyngoplasty (UPPP or UP3), and nasal operations are different types of surgeries that are also included.[50]

Interstitial Lung Disease (ILD)

ILDs are a general category that includes inflammatory and fibrotic infiltrative process of the lung; the interstitium, a part of the lungs’ anatomic structure (very thin lace-like network of tissue that extends throughout both lungs) that is often associated with collagen vascular disease in women and in many different lung conditions.[54] It provides support to the lungs’ microscopic air sacs (alveoli). Tiny blood vessels travel through the interstitium, allowing gas exchange between blood and the air in the lungs.[54],[55] There is some evidence that exposure to wood smoke may be associated with ILDs (lung fibrosis).[56] All forms of ILDs cause thickening of the interstitium are due to inflammation, scarring or extra fluid (edema), regular inhalation of dust, mold, or other irritants exposure.[33],[38],[57] Some forms of ILD are short-lived; others are chronic and irreversible. Regular exposures to inhaled irritants at work or during hobbies can also cause ILDs. Irritants are asbestos, silica, talc, metals, grains, and coal dusts including bird proteins.[57] Most ILD may affect women, but some of them have specific importance in women, including diseases those are specific of the female gender such as lymphangioleiomyomatosis, breast cancer or its treatment, idiopathic chronic eosinophilic pneumonia.[33],[38]

Lung cancer

Since the 1950s, lung cancer prevalence among women has increased worldwide by 500%. Since 1996, lung cancer mortality in women has surpassed annual breast cancer mortality, whereas lung cancer mortality rates have been decreasing in men.[58],[59] Lung cancer is often associated with smoking, but the disease can affect nonsmokers as well. Approximately 5% of lung cancer mortality in women has been linked to employment in occupational exposures. Women appear to be more susceptible to tobacco carcinogens in the development of lung cancer. Women usually smoke less and start smoking later than men.[7],[60] They may have increased activity of specific cytochromes, localized in the pulmonary tissue. How these mechanisms interact to result in the more readily developed lung cancer in women is, as yet, unclear. More attention needs to be addressed to the estrogen status of women patients with lung cancer, with regard to menopausal status, history or duration of birth-control pills or hormone replacement therapy (HRT), and actual smoking history during such medication, and as well as family history of smoking, cancer, and particularly lung cancer.[7],[61],[62]

The exposure to biomass smoke is a potential risk factor for lung cancer. Tobacco smoke is the most important risk for lung cancer and explains most cases in industrialized countries. Two-thirds of women with lung cancer are nonsmokers.[63] In developing countries, nonsmokers or passive smokers, frequently women, form a much larger proportion of patients with lung cancer. Odds ratios for lung cancer among women exposed to coal smoke at home, particularly that of so-called smoky coal.[10] Cooking with traditional biomass stoves is equivalent to smoking several cigarettes per day.[45],[63]

Tuberculosis (TB)

TB is a contagious bacterial infection that involves the lungs. It may spread to other organs also. Pulmonary tuberculosis is caused by the bacteria Mycobacterium tuberculosis.[12] Anyone can get TB by breathing in air droplets from a cough or sneeze of an infected person. TB is one of the infectious leading causes of female deaths in the world, killing over 1 million women every year, mainly in the reproductive age group of 15 to 44 years.[64],[65] TB was declared a public health emergency by World Health Organization in 1993 and has since continued to be a major cause of disability and death.[5],[66],[67] The disease is a significant contributor to maternal mortality and leading causes of death among women aged 15 to 45 years in high burden areas. Although underrecognition and underreporting of the disease in women due to socioeconomical and cultural factors may account for these differences, there is evidence to suggest that biological mechanisms, such as hormonal or genetic susceptibility differences, may also be responsible. The prevalence of tuberculous infection is similar between boys and girls aged <12 years. The progression from infection to disease is similar between the two genders aged <12 years; during adolescence and early adulthood, disease occurs predominantly among females.[26],[68]

Studies have shown that this disease affects women who have little power and autonomy in their households. Diagnosis and treatment of TB has not been equal.[69] Female Patients suffering from TB are reported to have psychiatric disorders such as depression, anxiety, psychosis, and also many psychosocial problems such as increased smoking and alcohol consumption, divorce, and isolation from the family.[70] Evidence suggests that these chronic exposures to smoke can weaken women’s respiratory systems, antibody production, local bronchial immunity, and impair the immune system’s ability to fight off bacteria.[43],[46]

Perception of illness has been found to vary with culture, ethnicity, education level, family structure, and socioeconomic differences. The nature and magnitude of TB among women is amazing. Certain aspects of poverty make women more susceptible to develop active TB. Cramped living conditions, overcrowding, and poor ventilation facilitate the spread of TB bacteria. TB poses a considerable risk for pregnant women and their babies.[9],[70] TB is best described as a doubled-edged sword, one blade being the effect of TB on pregnancy and the pattern of growth of the newborn, whereas the other is the effect of pregnancy on the progression of TB.[70],[71]

Social factors also contribute to the disparity in case detection between men and women. Unmarried females often search treatment from a far away healthcare center, because they fear that disclosure of the diagnosis could cause them problems in finding a partner for marriage. Extrapulmonary tuberculosis involvement is more common in women than in men.[72] To date, little has been performed to address gender disparities of TB and eliminate this disease as a leading killer of women.

Occupational lung diseases

An increase in occupational lung diseases in women has been identified in several studies, especially relating to occupational asthma and airway diseases.[73],[74] This may reflect increasing participation by women in occupations which were previously predominantly in males and may also in part reflect the increasing prevalence of cigarette smoking in women.[5],[20],[39] There is also evidence that airway aerosol deposition may be greater in larger airways in women than in men and that women may be more susceptible to developing chronic bronchitis. Predominantly female occupations with exposures relevant to occupational lung diseases include healthcare, laboratory animal workers, carpet, beedis, and fragrance sticks industries, domestic cleaners, textile workers, and pastry makers. Women in office buildings may develop building-related lung disease, including hypersensitivity pneumonitis and asthma, as well as respiratory symptoms as a component of sick-building syndrome.[42],[44] Employment of the husband or a household member in selected industries and occupations yielded significantly increased odds ratio, suggesting second-hand exposure may also be relevant to development of lung cancer in women, and those are frequently employed in casinos, bars, and other areas with second-hand tobacco smoke exposures.[38],[39]

The role of household exposure in lung disease in women: Household exposures can pose a risk for adverse respiratory effects whose burden is borne disproportionately among women, much of it preventable. Relevant exposure risks fall into three categories. Exposures may arise out of the routine household activities including cooking, cleaning, and laundering.[33],[42] Cooking can lead to exposure to particulate material and gases, each with potential adverse respiratory effects. Food preparation can also lead to allergic disease, including asthma associated with handling common foodstuffs.[42] To the extent that women spend more time indoors in these environments, they are at greater risk of adverse effects. Finally, sporadic yet important domestic exposures can occur through hobby or vocational activities, such as home maintenance or crafts work.[42],[43]

Pulmonary arterial hypertension (PAH)

Female predominance in PAH has been known for several decades and recent interest in the effects of sex hormones on the development of disease has substantially increased our understanding of this epidemiologic observation.[75] PAH is a severe clinical condition, characterized by a progressive increase of pulmonary vascular resistance leading to right ventricular failure and premature death. The significant increased incidence of PAH in females has been shown with the onset of puberty and shortly after delivery.[76] There have been cases in which HRT in obligate carriers of familial PAH seems to have triggered the manifestation of the disease. For these reasons, it has been hypothesized that female sex hormones could represent a trigger factor for the development of PAH.[77] The link between pregnancy and PAH is also uncertain. Recent human data have suggested that altered levels of estrogen, differential signaling, and altered metabolism of estrogens may underlie the gender difference in this disease.[77] Moreover, a large number of experimental studies are continuing, and there is great hope that it will not be long before more treatments are made available that potentially offer a cure for this disease.


A gender approach in health, while not excluding biological differences between women and men, considers the critical roles that social, cultural factors, and power relations between women and men play in promoting and protecting the health. This can be explained by differential risk of exposure to infection between women and men or by differences in susceptibility. In the majority of cases, the cause of this increased susceptibility is unknown. A female-related condition, that is, pregnancy, is associated with specific problems related to both the risks of transmission of the infection to the fetus and the risks of the antimicrobial treatment. Airway response to toxins (cigarette smoke, biomass fuels, and environmental pollutants) differs by gender based on the effects of female hormones on lung development and size, on regulation of receptors and biochemical pathways, and on airways’ hyperresponsiveness and inflammation. These differences appear to increase the susceptibility of postpubescent girls and women to asthma, COPD and lung cancer, as well as some respiratory infections, and infiltrative lung diseases. In addition, gender (social roles) exposes girls and women to higher levels of toxins from biomass fuel used for cooking and to particular occupational and chemical triggers.


I would also like to thank the faculty of Respiratory Medicine department for their immense support and co-operation.

Financial support and sponsorship

Financial support by Department of Science and Technology, New Delhi (DST/DISHA/SoRF PM/014/2013G) is acknowledged.

Conflicts of interest

There are no conflicts of interest.


1Parasuramalu BG, Huliraj N, Prashanth Kumar SP, Gangaboraiah XX, Ramesh Masthi NR, Srinivasa Babu CR. Prevalence of chronic obstructive pulmonary disease and its association with tobacco smoking and environmental tobacco smoke exposure among rural population. Indian J Public Health 2014;58:45-9.
2Samuel CO, Mohamed AG, Matthew RL. Advances in chronic obstructive pulmonary disease therapy: A vascular-targeted approach. Clin Med Insights Ther 2017;9:1179559×17719127.
3World Health Organization. Global tuberculosis report 2017. Geneva: World Health Organization; 2017. Available from: report/en/2017.
4Jha P, Peto R. Global effects of smoking, of quitting, and of taxing tobacco. N Engl J Med 2014;370:60-8.
5WHO. Tobacco fact sheet. Geneva: World Health Organization; 2015. Available from:
6Patel O, Syamlal G, Wood J, Dodd KE, Mazurek JM. Asthma mortality among persons aged 15–64 years, by industry and occupation—United States, 1999–2016. MMWR Morb Mortal Wkly Rep 2018;67:60-5.
7Thorgeirsson TE. A variant associated with nicotine dependence, lung cancer and peripheral arterial disease. Nature 2008;452:638-42.
8Loukola A, Hallfors J, Korhonen T, Kaprio J. Genetics and smoking. Curr Addict Rep 2014;1:75-82.
9Mishra P, Srivastava R, Krishnan A, Sreenivaas V, Pandav CS. Indoor air pollution-related acute lower respiratory infections and low birthweight: A systematic review. J Trop Pediatr 2012;58:457-66.
10Hoek G, Raaschou-Nielsen O. Impact of fine particles in ambient air on lung cancer. Chin J Cancer 2014;33:197-203.
11Das I, Jagger P, Yeatts K. Biomass cooking fuels and health outcomes for women in Malawi. Ecohealth 2017;14:7-19.
12Perumal R, Naidoo K, Padayatchi N. TB epidemiology: Where are the young women? Know your tuberculosis epidemic; know your response. BMC Public Health 2018;18:417.
13Torén K, Zock JP, Kogevinas M, Plana E, Sunyer J, Radon K et al. An international prospective general population-based study of respiratory work disability. Thorax 2009;64:339-44.
14Patel O, Syamlal G, Wood J, Dodd KE, Mazurek JM. Gender-related aspects in occupational allergies—Secondary publication and update. World Allergy Organ J 2017;10:44.
15Raulf M, Brüning T, Jensen-Jarolim E, van Kampen V. Asthma is different in women. Curr Allergy Asthma Rep 2015;15:28.
16Lang I, Meyer BC, Ogo T et al. Balloon pulmonary angioplasty in chronic thromboembolic pulmonary hypertension. Eur Respir Rev 2017;26:1-15; 160119. 16000617.0119-2016.
17Gibson J, Loddenkemper R, Lundbäck B, Sibille Y. Respiratory health and disease in Europe: the new European Lung White Book. European Respiratory J. 2013. 42: 559-63. doi: 10.1183/09031936.00105513.
18Jia J, Conlon TM, Sarker RS, Taşdemir D, Smirnova NF, Srivastava B et al. Cholesterol metabolism promotes B‐cell positioning during immune pathogenesis of chronic obstructive pulmonary disease. EMBO Mol Med 2018; 10: e8349.
19Kant S. Socio-economic dynamics of asthma. Indian J Med Res 2013;138:446-8.
20Reddel HK, Bateman ED, Becker A, Boulet LP, Cruz AA, Drazen JM et al. A summary of the new GINA strategy: A roadmap to asthma control. Eur Respir J 2015;46:622-39.
21Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for diagnosis, management and prevention of COPD. 2016. Available from:
22Pelissier S, Chaboillez S, Téolis L, Lemiere C. Outcome of subjects diagnosed with occupational asthma and work-aggravated asthma after removal from exposure. J Occup Environ Med 2006;48:656-9.
23Henneberger PK, Mirabelli MC, Kogevinas M, Antó JM, Plana E, Dahlman-Höglund A et al. The occupational contribution to severe exacerbation of asthma. Eur Respir J 2010;36:743-50.
24Kant S, Ojha S. Management of asthma in pregnancy. Indian J Allergy Asthma Immunol 2006;20:117-20.
25Kant S, Ojha S, Verma SK. Pregnancy and asthma. J Obes Gynaecol Today 2007;12:226-30.
26Kant S, Srivastava K. Tuberculosis: : Female genital tract. Lucknow Med J 2012;2:94;101-5.
27Blanc PD. Occupation and COPD: A brief review. J Asthma 2012;49:2-4.
28Paulin LM, Diette GB, Blanc PD, Putcha N, Eisner MD, Kanner RE et al. Occupational exposures are associated with worse morbidity in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2015;191:557-65.
29Miravitlles M, Vogelmeier C, Roche N, Halpin D, Cardoso J, Chuchalin AG et al. A review of national guidelines for management of COPD in Europe. Eur Respir J 2016;47:625-37.
30Lytras T, Kogevinas M, Kromhout H, Carsin AE, Antó JM, Bentouhami H et al. Occupational exposures and 20-year incidence of COPD: The European Community Respiratory Health Survey. Thorax 2018; 0:1-8. doi: 10.1136/thoraxjnl-2017-211158.
31Dherani M, Pope D, Mascarenhas M, Smith KR, Weber M, Bruce N. Indoor air pollution from unprocessed solid fuel use and pneumonia risk in children aged under 5 years: A systematic review and meta-analysis. Bull World Health Organ 2008;86:390-8.
32Choi JY, Baumgartner J, Harnden S, Alexander BH, Town RJ, D’Souza G et al. Increased risk of respiratory illness associated with kerosene fuel use among women and children in urban Bangalore, India. Occup Environ Med 2015;72:114-22.
33Accinelli RA, Llanos O, Lopez LM, Pino MI, Bravo YA, Salinas V et al. Adherence to reduced-polluting biomass fuel stoves improves respiratory and sleep symptoms in children. BMC Pediatrics 2014;14:1-12.
34Agrawal S, Yamamoto S. Effect of indoor air pollution from biomass and solid fuel combustion on symptoms of preeclampsia/eclampsia in Indian women. Indoor Air 2015;25:341-52.
35Hobbs BD, de Jong K, Shrine NRG, Wyss AB, London SJ, Cho M. A genome-wide association study of chronic obstructive pulmonary disease identifies 22 risk loci. Nat Genet 2017;49:426-32.
36Diaz E, Smith-Sivertsen T, Pope D, Lie RT, Diaz A, McCracken J et al. Eye discomfort, headache and back pain among Mayan Guatemalan women taking part in a randomized stove intervention trial. J Epidemiol Commun Health 2007;61:74-9.
37Nicholas RA, John EC, Robert PM. Smoking and lung function of lung health study participants after 11 years. Am J Respir Crit Care Med 2002;166:675-9.
38Obeidat ME, Ding X, Fishbane N, Hollander Z, Ng RT, McManus B et al. The effect of different case definitions of current smoking on the discovery of smoking-related blood gene expression signatures in chronic obstructive pulmonary disease. Nicotine Tob Res 2016;18:1903-9.
39Bossé Y, Postma DS, Sin DD, Lamontagne M, Couture C, Gaudreault N et al. Molecular signature of smoking in human lung tissues. Cancer Res 2012;72:3753-63.
40Fatmi Z, Coggon D, Kazi A, Naeem I, Kadir MM, Sathia Kumar N. Solid fuel use is a major risk factor for acute coronary syndromes among rural women: A matched case control study. Public Health 2014;128:77-82.
41Fullerton DG, Bruce N, Gordon SB. Indoor air pollution from biomass fuel smoke is a major health concern in the developing world. Trans R Soc Trop Med Hyg 2008;102:843-51.
42Fullerton DG, Suseno A, Semple S, Kalambo F, Malamba R, White S et al. Wood smoke exposure, poverty and impaired lung function in Malawian adults. Int J Tuberc Lung Dis 2011;15:391-8.
43Forouzanfar MH, Alexander L, Anderson HR, Bachman VF, Biryukov S, Brauer M et al. Global, regional, and national comparative risk assessment of 79 behavioral, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990–2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;386:2287-323.
44Gajalakshmi V, Peto R. Smoking, drinking and incident tuberculosis in rural India: Population-based case–control study. Int J Epidemiol 2009;38:1018-25.
45Grabow K, Still D, Bentson S. Test kitchen studies if indoor air pollution from biomass cookstoves. Energy Sustain Dev 2013;17:458-62.
46Sehgal M, Rizwan SA, Krishnan A. Disease burden due to biomass cooking-fuel-related household air pollution among women in India. Glob Health Action 2014;7:25326.
47Gurley ES, Homaira N, Salje H, Ram PK, Haque R, Petri W et al. Indoor exposure to particulate matter and the incidence of acute lower respiratory infections among children: A birth cohort study in urban Bangladesh. Indoor Air 2013;23:379-86.
48Vakulin A, Yap C, Doug McEvoy R, Li Chai-Coetzer C. Obstructive sleep apnoea: Therapeutic options and challenges. Clin Med Insights Ther 2017;9:1179559X17711932.
49Elshaug AG, Moss JR, Southcott AM, Hiller JE. Redefining success in airway surgery for obstructive sleep apnea: A meta analysis and synthesis of the evidence. Sleep 2007;30:461-7.
50Motamedi KK, McClary AC, Amedee RG. Obstructive sleep apnea: A growing problem. Ochsner J 2009;9:149-53.
51Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Rein J, Vela-Bueno A et al. Prevalence of sleep-disordered breathing in women: Effects of gender. Am J Respir Crit Care Med 2001;163:608-13.
52Kitakata H, Kohno T, Fukuda KJ. Sleep-disordered breathing in the elderly: Is it distinct from that in the younger or middle-aged populations? Thorac Dis 2018;10:S1102-7.
53Mylvaganam R, Dua S, Nelson-Piercy C, Mathur A. Interstitial lung disease in women of child-bearing age. Semin Respir Crit Care Med 2017;38:185-90.
54Furukawa H, Oka S, Shimada K, Tsuchiya N, Tohma S. Genetics of interstitial lung disease: Vol de Nuit (Night Flight). Clin Med Insights Circ Respir Pulm Med 2015;9:1-7.
55Hyldgaard C. A cohort study of Danish patients with interstitial lung diseases; burden; severity; treatment and survival. Dan Med J 2015;62:B5069.
56Benowitz NL. Nicotine addiction. N Engl J Med 2010;362:2295-303.
57Olsson AC, Vermeulen R, Schuz J, Kromhout H, Pesch B, Peters S et al. Exposure–response analyses of asbestos and lung cancer subtypes in a pooled analysis of case–control studies. Epidemiology 2017;28:288-99.
58Ali M, Jawad M. Health effects of waterpipe tobacco use: Getting the public health message just right. Tob Use Insights 2017;10:1179173X17696055.
59Prakash V, Singh A, Kant S, Verma AK, Saxena P, Bhatia A. A comparison of toxicity profile of gemcitabine monotherapy versus etoposide/cisplatin in the treatment of locally advanced or metastatic non-small cell lung cancer. Int J Basic Clin Pharmacol 2015;4:70-4.
60Raaschou-Nielsen O, Andersen ZJ, Beelen R, Samoli E, Stafoggia M, Weinmayr G et al. Air pollution and lung cancer incidence in 17 European cohorts: Prospective analyses from the European Study of Cohorts for Air Pollution Effects (ESCAPE). Lancet Oncol 2013;14:813-22.
61Josyula S, Lin J, Xue X, Rothman N, Lan Q, Rohan TE et al. Household air pollution and cancers other than lung: A meta-analysis. Environ Health 2015;14:24.
62Seow WJ, Hu W, Vermeulen R, Hosgood HD III, Downward GS. Household air pollution and lung cancer in China: A review of studies in Xuanwei. Chin J Cancer 2014;33:471-5.
63Hawkes S, Buse K. Gender and global health: Evidence, policy, and inconvenient truths. Lancet 2013;381:1783-7.
64Horton KC, MacPherson P, Houben RMGJ, White RG, Corbett EL. Sex differences in tuberculosis burden and notifications in low- and middle-income countries: A systematic review and meta-analysis. PLoS Med 2016;13:e1002119.
65Kant S, Maurya AK, Kushwaha RAS, Nag VL, Prasad R. Multi-drug resistant tuberculosis: An iatrogenic problem. Biosci Trends 2010;4:39–47, 48-55.
66Prasad R, Gupta N, Banka A. Multi drug resistant tuberculosis/rifampicin-resistant tuberculosis: Principles of management. Lung India 2018;35:78-81.
67Dodd PJ, Looker C, Plumb I, Bond V, Schaap A, Shanaube K et al. Age- and sex-specific social contact patterns and incidence of Mycobacterium tuberculosis infection. Am J Epidemiol 2016;183:156-66.
68Nhamoyebonde S, Leslie A. Biological differences between the sexes and susceptibility to tuberculosis. J Infect Dis 2014;209(Suppl 3):S100-6.
69Wong JM, Nyachieo DO, Benzekri NA, Cosmas L, Ondari D, Yekta S et al. Sustained high incidence of injuries from burns in a densely populated urban slum in Kenya: An emerging public health priority. Burns 2014;40:1194-200.
70Lin HC, Chen SF. Increased risk of low birth weight and small for gestational age infants among women with tuberculosis. BJOG 2010;117:585-90.
71Perez-Padilla R, Schilmann A, Riojas-Rodriguez H. Respiratory health effects of indoor air pollution. Int J Tuberc Lung Dis 2010;14:1079-86.
72Patel S, Louis JM. Obstructive sleep apnoea in pregnancy—More questions than answers. Eur Endocrinol 2013;9:121-4.
73Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med 2014;370:640-9.
74Pugh ME, Hemnes AR. Pulmonary hypertension in women. Expert Rev Cardiovasc Ther 2010;8:1549-58.
75Minai OA, Nathan SD, Hill NS, Badesch DB, Stoller JK. Pulmonary hypertension in lung diseases: survey of beliefs and practice patterns. Respir Med. 2010; 104:741-8.
76Dempsie Y, MacLean MR. The influence of gender on the development of pulmonary arterial hypertension. Exp Physiol 2013;98:1257-61.
77Galiè N, Humbert M, Vachiery JL, Gibbs S, Lang I, Torbicki A et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). Eur Heart J 2016;37:67-119.