The Association between Chronic Heroin Smoking and Chronic Obstructive Pulmonary Disease

Abstract

Introduction:

Little is known about the correlation between chronic obstructive pulmonary disease (COPD) and heroin smoking. Heroin smoking is a recent underinvestigated problem. The goal of this study is to study the impact of heroin smoking among COPD patients.

Methods:

This is a descriptive clinical study. A combination of self-reporting questionnaires and data extraction tools were used to collect information during baseline tests, interviews, and follow-ups. Patients' medical, clinical, and socioeconomic history were recorded. Participants were recruited using random sampling from multiple centers.

Results:

Out of 1034 COPD patients, heroin smokers represented the vast majority of addiction cases (n = 133). Heroin smokers were leaner than non-addicts (19.78 ± 4.07 and 24.01 ± 5.6, respectively). The most common type of comorbidities among heroin smokers was emphysema (27%). Both the forced expiratory volume (FEV₁)/forced vital capacity ratio and FEV1% predicted were lower among heroin smokers than non-addicts (52.79 ± 12.71 and 48.54 ± 14.38, respectively). The majority of heroin smokers (55%) had advanced COPD, and at least 15% of heroin smokers suffered from frequent respiratory failure. The mean ± SD for COPD onset age among heroin smokers was 44.23 ± 5.72, and it showed a statistically significant correlation (P < 0.001).

Conclusion:

Heroin smoking might be linked to the onset of COPD. Heroin smokers showed a significantrespiratory impairment compared to tobacco smokers of the same age group.

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is a chronically progressive lung disease commonly characterized by a chronic and productive cough, wheezing, shortness of breath, and chest tightness.[1] COPD is an umbrella term that might encompass multiple overlapping lung diseases or disorders, including chronic bronchitis, bronchiectasis, bronchial asthma, and emphysema. COPD can be distinguished from other conditions by a progressive obstructive limitation of airflow during expiration that can be irreversible.[2,3]

COPD is commonly diagnosed by following the Global Initiative for COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD]) guidelines.[3] The GOLD standard is based on the assessment of spirometry results and the evaluation of the present signs symptoms, history, and risk factors; GOLD classification of COPD severity consists of four categories from I to IV.[4] Spirometry is essential to make a clinical diagnosis; a post-bronchodilator forced expiratory volume (FEV1)/forced vital capacity (FVC) <0.70 defines the persistent limitation in airflow.[4]

Heroin (diacetylmorphine) is an extremely addictive illicit drug. Heroin is a processed product derived from morphine extracted from the opium poppy, a plant originating from the Middle East and Southeast Asia.[5] Heroin is usually adulterated (cut) by dealers or producers with many bulking agents such as starch powder, powdered milk, quinine, and even meat tenderizer powder.[5,6] Heroin was chemically synthesized in 1874 by the founder of the Royal Institute of Chemistry (Charles Romley Alder Wright) in the UK. It was then resynthesized by a German chemist named Felix Hoffmann at Bayer Pharmaceuticals in Germany; it was officially registered in June 1898. It was marketed as a non-addictive cough suppressant and over-the-counter analgesic drug that is safer to use than morphine.[7,8,9] In 1913, Bayer ceased heroin production due to its addictive effect.[5]

Heroin smoking started around the first quarter of the 20^th century in Shanghai, east of China. Smoking heroin is considered among the fastest routs of administration with almost instant effect.[10,11] The first method of smoking heroin was heating the heroin powder in porcelain bowls or bamboo tubes as shown in Figure 1.[12,13] Smoking heroin was spread throughout all East Asian countries and to the USA and Europe by the next decade.[11]

Figure 1.

(a) A Chinese bamboo opium pipe with ivory terminals and brass sucking tube used for smoking heroin. (b) A Chinese immigrant in an opium den puffs on a pipe while holding a cat in San Francisco, USA.

The smoking techniques for heroin were refined and simplified in Hong Kong during the 1950s. The new method depends on heating the drug mix on a simple tinfoil above a gentle fire flame and inhaling the produced vapors by a simple glass tube. The new way was so simple and required no special equipment; it was spread quickly all over the world by the end of the 1970s.[11] Smoking heroin was nicknamed “Chasing the Dragon,” which refers to the careful chasing and inhaling of the produced fumes when gently moving the liquid to prevent it from overheating and burning quickly.[14]

Little is known about chronic heroin smoking's effect on the lungs.[15,16] The correlation between smoking heroin and the onset of COPD remains exceptionally vague and unclear due to the lack of research on heroin smokers. In this research, we focused on the association between chronic smoking of heroin and COPD. We investigated the early onset of COPD among heroin smokers, and the effect of heroin smoking on COPD patients' lungs.

METHODS

Study design

This study is a part of a larger research project that focuses on COPD. It is a descriptive investigative longitudinal study that combines both retrospective and prospective clinical analysis, and it was conducted in Penang, Malaysia. This study also included specific biomarker analysis; which was postponed for a few months due to lock-down and covid-19 outbreak.

Settings

This is a multi-center study conducted in the northern region of Malaysia. All health-care facilities are run publicly by the Ministry of Health, Malaysia. Cases were identified from the record and traced back to confirm substance abuse history from Methadone Clinics and to build a unique medical profile for each case. A psychologist and a pulmonologist from the Ministry of Health and a clinical research investigator from University Sains Malaysia organized and coordinated meetings and follow-up sessions.

Participants

Cases were recruited on the basis of the results, available record, and history and based on the inclusion criteria. Then, they were invited to baseline tests and interview. All the included patients were examined by competent pulmonologists and had a confirmed diagnosis of COPD. Written confirmed consent was taken from each participant after the introduction to the study's details. Then, regular appointments were booked based on the patients' convenience. Those missing their appointments were reminded and were given multiple chances to make a new one in 9 months; otherwise, they will be considered as a dropout.

Tests and data collection

Complete demographics, patients' medical history, socioeconomic data, and detailed clinical history were taken, including lifestyle, habits, smoking history, drug use history, Modified Medical Research Council (mMRC) dyspnea scores, COPD Assessment Test (CAT) scores, spirometry results, GOLD's COPD severity, exacerbations history, and comorbidities. A combination of self-reporting questionnaires and data extraction tools were used to record results and detailed history during baseline tests, interviews, and follow-ups. For health screening and testing, patients were requested not to take any short-acting bronchodilator 8 h before the visit or any long-acting bronchodilator 24 h before the visit. For those who took bronchodilator, only post-bronchodilator spirometry was performed. Suspected emphysema cases were detected based on signs and symptoms, chest X-rays, computed tomography scan (if X-rays results were inconclusive), and most importantly, pulmonary function test.

All the included patients were required to complete the baseline tests, clinical interviews, and at least two follow-ups in 9 months after the baseline. Monitoring and follow-ups for each patient were planned for 1 year. We focused on participants who were able to complete the spirometry test, which was conducted by a well-trained staff member and completed according to the American Thoracic Society guidelines;[17] we tried to take an average of two or three readings to get more accurate results.

Sample and sample size

We tried to recruit the highest possible number of patients with COPD and heroin smoking history. All recruited cases met the criteria of the GOLD as per the 2019 report.[4] Cases were also evaluated, classified, and stratified on the basis of severity and comorbidities, and the impact of risk factors was analyzed.

Inclusion and exclusion criteria

All male COPD patients above 35 years of age who were hospitalized or visited the clinics were included in the study (we have recruited only male subjects because this research is a part of a larger project and some of the biomarkers that we are analyzing can be affected by postmenopausal hormonal changes). COPD patients who are active users, currently withdrawing, or ex-users were also included. Patients with high-risk factors profile and patients with alpha-1 antitrypsin deficiency were excluded. Female patients were excluded to eliminate the hormonal effects as a lurking factor. Unique populations of patients with conditions such as cancerous diseases, hepatic malfunction, severe metabolic disorders, and mastocytosis were excluded; endocrinal disorders such as Addison's disease, Cushing's syndrome, and Graves' disease were also excluded due to the drastic impact of this kind of diseases on patients' health. COPD patients with TB history were also excluded unless they were successfully treated at least 5 years ago.

Statistical analysis

Statistical analyses were made using the latest version of the Statistical Package for the Social Sciences (SPSS 24, Inc., Chicago, IL, USA). Descriptive statistics were made to determine the nature of the study population. A paired t-test and Chi-square were made to evaluate the changes in two points. Correlation analysis was conducted to evaluate the strength of the relationship between two quantitative variables. A linear and logistic regression tests were performed to estimate the effect of various factors and to detect the interactions between variables. Statistical significance was tested at the conventional 5% level.

Ethical approval

This study was registered with the National Medical Research Register with the following number: NMRR-19-239-46017. Ethical approval was obtained from all relevant committees and the Medical Research and Ethics Committee, Ministry of Health Malaysia, with the following number: KKM/NIHSEC/P19-528.

RESULTS

Subjects recruitment

More than 30,500 cases were screened, and 1034 were recruited [Figure 2]. Out of 1034 COPD patients, 220 patients were drug users (heroin, morphine, cocaine, and alcohol), and heroin smokers represented the vast majority of them, with 133 (60.4%) patients representing almost 13% of all recruited cases. Nearly 90% (119) of heroin smokers reported that they had tried other drugs such as morphine, cannabis, and cocaine at least once, and one-third of them started with other drugs then shifted to heroin. Furthermore, a very significant number of patients tried the intravenous route for heroin at least once, representing 25.5% (34) of all heroin smokers.

Figure 2.

The flowchart of search, screening, and recruitment process

Demographics and data analysis

Heroin smokers were generally leaner than the average patient, and almost one-third of them were underweight, and some were very severely underweight. The lowest body mass index (BMI) encountered in the study was a Chinese heroin smoker with BMI of 12.40 kg/m². Furthermore, some differences among ethnic groups were observed in BMI and age. For example, Chinese patients were more physically fit and were older than other ethnic groups, while obesity was the most common among Indian patients.

The majority of heroin smokers were categorized in Group A (below the official poverty line in Malaysia; monthly income of <2000 Malaysian Ringgit) with more than 58%. In terms of respiratory comorbidities, 27% of heroin smokers suffered from emphysema which showed a significant association with heroin smoking (P < 0.001), while asthma was the most prevalent respiratory comorbidity among non-addicts patients [Table 1].

Table 1.

Overall demographics and respiratory parameters among addicts and nonaddicts chronic obstructive disease patients

	Addicts				Nonaddicts	Overall
	Heroin	Morphine	Cocaine	Alcohol
Patient (male)	133	14	4	69	814	1034
Age (years)	53.93±7.67#	59.01±6.8	57.83±3.51	67.33±11.3	69.91±10.92	61.60±8.04
BMI (kg/m2)	19.78±4.07	22.91±5.01	23.16±5.82	22.51±5.03	24.01±5.6	22.47±5.1
Average income	A (58.6)*	B (57.1)*	A (50)*	C (62.3)*	B (59.1)*	B (48)*
Comorbidities	99 (74.4)*	5 (35.7)*	2 (50)*	50 (72.4)*	735 (90.2)*	891 (86.1)*
Asthma	8	3	1	24	279	315
Emphysema	36#	-	-	-	101	137
Bronchitis	19	2	1		116	145
Bronchiectasis	29	-	-	76	186	221
URTI/LRTI	7	-	-	13	53	73
FEV1/FVC ratio	52.79±12.71#	66.35±8.15	63.89±16.6	64.16±14.56	65.10±16.5	62.45±13.7
FEV1% pred	48.54±14.38#	59.46±15.3	62.3±12.44	69.46±16.38	56.46±17.58	59.24±15.21
SpO2%	95#	97	97	96	97	96
mMRC Dyspnea Scale	129 (97)*,#	13 (92.8)*	1 (25)*	65 (94.2)*	751 (92.2)*	944 (91.2)*
Grade 0	1	5	-	11	51	68
Grade 1	51	6	1	19	426	503
Grade 2	61	2	-	22	245	330
Grade 3	13	-	-	2	17	32
Grade 4	3	-	-	-	8	11
CAT score	108 (81.2)*	11 (78.6)*	2 (50)*	41 (59.4)*	721 (88.5)*	883 (85.4)*
>10	67	10	2	29	560	668
≤10	41	1	-	12	161	215
Exacerbations (years)	0.8±0.5	0.7±0.5	-	1±0.5	0.7±0.3	0.8±0.4
COPD severity	129 (96.9)*,#	5 (35.7)	1 (25)*	59 (85.5)*	775 (95.2)*	969 (93.8)*
Stage-I	11	2	-	15	170	198
Stage-II	45	3	1	35	331	415
Stage-III	69	-	-	9	231	309
Stage-IV	4	-	-	-	43	47
Rehab pts	6 (0.45)*	-	-	3 (4.3)*	84 (10.3)*	93 (8.9)*
LTOT	2 (0.15)*	-	-	-	124 (15.2)*	126 (12.1)*
Defaulters	54 (40.6)*,#	4 (28.5)*	-	6 (8.6)*	78 (9.6)*	146 (14.1)*
ARF	20 (15)*	2 (2.8)*	-	6 (8.7)*	110 (13.5)*	138 (13.3)*
Type-I	6	-	-	-	30	36
Type-II	14	2	-	6	80	102

*Number and/or percentage from the indicated column, ±: SD, ^#Statistically significant when compared to nonaddicts tobacco smokers (P<0.001). BMI: Body mass index, A: Average income below the national poverty line, B: Average income 2000-5000 RM per month, C: Average income 5000-1000 RM per month, Defaulters: Patients who fail to complete the course of medical treatment. FEV1: The first second of forced expiration, FVC: Forced vital capacity, FEV₁% pred: The predicted first second of forced expiration, mMRC: Modified Medical Research Council Dyspnea Scale, CAT: COPD assessment test, Rehab Pts: Pulmonary rehabilitation patients, LRTI: Lower respiratory tract infections, LTOT: Long-term oxygen treatment, ARF: Acute respiratory failure, URTI: Upper respiratory tract infections, COPD: Chronic obstructive pulmonary disease, SD: Standard deviation

The youngest patient was 38 years old, while the oldest one was 98 years old. Heroin smokers had a significantly younger age than non-heroin smokers (53.93 ± 7.67 VS 69.91 ± 10.92, P < 0.001). A statistically significant association was observed between heroin smoking and COPD (P < 0.001).

On average, both the FEV1/FVC ratio and FEV₁% predicted were lower among heroin smokers than non-addicts, with 52.79 ± 12.71 and 48.54 ± 14.38, respectively. Heroin smokers showed a significant decline in the FEV1 means and their oxygen saturation (P < 0.001). The vast majority of cases assessed with the mMRC dyspnea scale were clustering in the first and second grades with 833 cases, and patients in the third grade represented around 10% of heroin smokers. At the same time, they occupied only 2.1% of the non-addicts group. More than 75% of patients were above ten on CAT score out of 883 cases. Exacerbation frequency showed no significant difference among various groups; however, exacerbations triggered by upper respiratory tract infection were more common among patients addicted to alcohol, whereas those triggered by lower respiratory infections were slightly more prevalent among heroin smokers.

More than 86% of heroin smokers had a history of tobacco smoking, and 91% of non-addicts reported a history of smoking tobacco. Almost 14% of heroin smokers reported being irregular tobacco smokers or smoking one or two cigarettes per day. After linear regression analysis, a statistically significant association between heroin smoking and reduced FEV₁ was observed (P < 0.001), and the logistic regression analysis for dyspnea prevalence and smoking heroin showed an association between both of them.

Around 50% of heroin smokers were classified as stage-III or Stage-IV borderline COPD patients, while among non-addicts, the most significant number of patients was in stage-II COPD with 331 cases. More than 10% of nonaddicts needed pulmonary rehabilitation treatment at least once, which was as double as in heroin smokers, and long-term oxygen therapy was less commonly prescribed for addicts. Unfortunately, more than one-third of heroin smokers were frequent defaulters (who did not complete the course of medical treatment), especially those who were active users, while defaulters among non-addicts represented <10%. More than 13% of patients suffered from acute exacerbations in COPD that led to acute respiratory failure at least once, and the majority of respiratory failure cases were type-II. There was no significant difference between drug users and non-drug users.

Heroin smoking and the onset of chronic obstructive pulmonary disease

The onset age for COPD among heroin smokers was significantly lower than the non-addicts group. The mean SD for onset age among heroin smokers was 44.23 ± 5.72, whereas it was 61.82 ± 9.72 for non-addicts patients, and a statistically significant correlation has been observed between the early onset of COPD (ages from 36 up to 55) and chronic heroin smoking (P < 0.001). More than one third of chronic heroin smokers developed COPD at younger age (before 46), while the onset age for 80% of non-heroin smokers was after 56 years of age, [Figure 3].

Figure 3.

Heroin smoking linked to the early age of chronic obstructive pulmonary disease in the terms of patient's number (P < 0.001)

The annualized progression of COPD among heroin smokers showed significant results. Symptoms such as dyspnea increased significantly, reaching a mean ± SD of 3 for mMRC among heroin smokers (P < 0.001) in the final follow-up, while no significant change has been observed for tobacco smokers of the same age group. A significant reduction has been observed in FEV1% predicted and in the FEV1/FVC ratio for heroin smokers [Table 2]. The mean ± SD for CAT score showed a significant decline, while a reduction in SpO₂% value was observed among heroin smokers with very little significance (P < 0.049).

Table 2.

Annualized progression of chronic obstructive pulmonary disease among heroin smokers

Variable	Baseline	Final follow-up	P
FEV1% pred
H. smokers	52.12±15.45	42.30±14.87	<0.001*,†
T. smokers	66.78±16.34	70.86±16.2	0.728*
FEV1/FVC ratio
H. smokers	56.72±16.89	48.8±15.18	0.018*,†
T. smokers	69.18±16.44	68.76±16.7	0.567*
mMRC score
H. smoker	2.52±0.78	2.98±0.89	<0.001*
T. smoker	2.1±0.47	2.12±0.63	0.683*
CAT score
H. smokers	16.79±7.21	13.28±6.78	0.036*
T. smokers	17.42±7.89	17.79±8.11	0.712*
Spo2 (%)
H. smokers	96±0.94	94.11±0.86	0.049*
T. smokers	96.38±0.79	96.32±0.90	0.689*

*Paired samples correlation comparing means for baseline and final follow-ups, ^†Significant independent t-test for heroin and tobacco smokers (P<0.001) ±: SD, FEV1: The first second of forced expiration, FVC: Forced vital capacity, FEV₁% pred: The predicted first second of forced expiration, H. Smokers: Heroin smokers, CAT: COPD assessment test, mMRC: Modified Medical Research Council Dyspnea Scale, T. Smokers: Tobacco smokers, COPD: Chronic obstructive pulmonary disease, SD: Standard deviation

After running predictor variable analysis, we found that, even though FEV1% predicted and FEV1/FVC ratios were significantly lower and showed a significant decline among heroin smokers during the study, heroin smoking was not a good predictor for that decline (P < 0.373 and P < 0.871, respectively). In contrast, for factors such as onset age, patients' BMI, and mMRC scores, it was a significant predictor (P < 0.001). The logistic regression indicated that heroin smokers were at higher risk of getting COPD at younger ages (1.354) as compared with tobacco smokers (95% CI: 1.117 to 1.591, P < 0.001) [Table 3]. Furthermore, heroin smokers were more likely to get lower BMI, mMRC scores, and CAT scores, while the effect on GOLD categories and for the patients' race was not significant.

Table 3.

Logistic regression for high-risk variables

Variable	Crude OR (95% CI)	P
Race
Malay	1
Chinese	0.977 (0.764-1.191)	0.778
Indian	0.913 (0.741-1.124)	0.391
Onset age (years)	1.354 (1.117-1.591)	0.001*
BMI (kg/m2)	1.286 (1.201-1.371)	0.001*
mMRC Scale	1.104 (1.023-1.186)	0.001*
GOLD category	0.994 (0.799-1.082)	0.813
CAT score	1.026 (1.023-1.029)	0.001*

*P<0.001. BMI: Body mass index, CAT score: COPD assessment test score, GOLD: The global initiative for chronic obstructive lung disease, mMRC: Modified Medical Research Council Dyspnea Scale, OR: Odds ratio, CI: Confidence interval, COPD: Chronic obstructive pulmonary disease

DISCUSSION

The number of heroin smokers among COPD patients was more significant than alcohol-dependent patients even though alcohol is easily accessible, cheaper, does not require dangerous contact with drug cartels, and does not have the same social stigma. This can be attributed to many factors; for example, heroin is abundantly available in Malaysia due to the geographic proximity sharing borders with Thailand, which is a major hub for opiate trade and a part of the “opiate golden triangle” where a massive amount of opium is being produced and smuggled since the 1950s.[18] Furthermore, alcohol addiction can be underreported since patients underestimate their consumption and do not report it accurately and overestimate their capacity to stop when needed.[19] Furthermore, heroin presents more than 60% of all recorded illegal drug use cases in Malaysia.[21] By far, smoking heroin was the route of choice among users and has been on a global rise since the 1960s as compared to other routes of administration,[22,23] which complies with the findings presented in this manuscript.

Heroin smokers had significantly lower BMI than other groups and non-addicts (P < 0.001). It has been observed that COPD patients were leaner than the general population and to non-addicts, which is entirely in harmony with the findings of Bitar et al. and Guo et al.[24,25] The results also showed an association between low BMI and chronic heroin smoking, where almost one-third of the subject have BMI below 18; Buster and his colleagues came to similar results, with 26% of participants being underweight.[15] Furthermore, it has been observed that unlike diabetes and cardiovascular diseases, among COPD patients, there is an inverse relationship between BMI and the risk of mortality, also known as the “BMI Paradox.”[26,27]

The number of patients with emphysema among heroin smokers was significantly higher than in other groups. This can be assigned to the damage caused by ingesting a combination of hot toxic fumes produced by smoking heroin, leading to an early onset of emphysema among heroin smokers.[28,29] Furthermore, the adulteration of heroin with bulking agents such as talc and clenbuterol was linked to the early onset of emphysema due to elastin degradation in the lungs' vascular wall extracellular matrix.[30] A recent cohort study conducted by Walker et al. found that smoking heroin was correlated to the early COPD onset, especially the emphysema phenotype.[28]

The FEV₁% predicted among heroin smokers was lower than other COPD patients, and the onset age of COPD was significantly lower than the non-addicts group. According to Walker et al., patients who were chronic heroin smokers had a 31.5% lower FEV₁% predicted with mean FEV₁/FVC of 0.4. The only difference in obstruction measured by the FEV₁/FVC ratio was attributed to the degree of lung function impairment since more severe patients have severely reduced lung function, more symptoms, and more frequent follow-up visits.[28]

In the Netherlands, Buster et al. found that heroin smokers on methadone treatment have an impaired lung function and a reduced FEV₁% predicted and FEV₁/FVC ratio was associated with more frequent episodes of dyspnea.[15] This is homogenous with our findings since we have observed reduced spirometry and a declining breathing ability among heroin smokers; however, the number of exacerbations requiring hospitalization per year showed that no significant difference between addicts and non-addicts could be explained by less reporting of exacerbation among heroin smokers.

Heroin smokers were suffering from more severe breathing difficulties, and a significant number of them were classified as third and fourth grades on the mMRC dyspnea scale, and there was a significant association between smoking heroin and more severe dyspnea among the patients (P < 0.01). Lewis-Burke et al. concluded that smoking heroin is linked to impaired lung function; they reported that the Medical Research Council scores were higher among COPD patients with a history of heroin smoking and their lung condition was worse than the control group.[30] Severe dyspnea and a decline in lung function among heroin smokers were observed in this project. This finding comes in parallel to a very recent report from the UK, where the researchers noticed a rapid decline in FEV1 and a significant increase in respiratory symptoms among heroin smokers, which seems to be persistent even among ex-users.[31] Furthermore, chronic heroin smokers were at higher risk of developing COPD because of the high prevalence and the lower age average than tobacco smokers of the same age.[32]

The mechanism of COPD progression among heroin smokers is not clear and still mysterious. Some researchers suggested that the hot toxic fumes inhaled by heroin smokers can trigger an inflammatory response, which leads to excessive mucus production, which is associated with increased oxidative stress, bronchitis, and intra-alveolar elastin damage due to activated heat protein denaturation, which is linked typically to emphysema.[15,33] Furthermore, heroin is usually adulterated with compounds such as caffeine, phenolphthalein, chalk, talcum powder, chloroquine, paracetamol, starch, and meat tenderizers that produce toxic fumes on burring,[35] which can increase the lungs' inflammatory response leading to conditions like bronchitis, early onset of COPD, and to the development of leukoencephalopathy.[30] Besides that, some research suggests that the Valsalva maneuver, which is usually performed by heroin smokers to enhance absorption of the drug, can cause damage deep within the lung due to trapped hot fumes and contaminants overload.[35] Furthermore, it has been found that frequent exposure to opiates such as heroin can elevate histamine and tryptase levels compared to the control group. However, according to the researchers, the observed allergic symptoms were mild and did not require clinical interventions.[36]

Many heroin smokers in our study lived in dire conditions and were extremely difficult to reach, which widened the gap and increased health-care inequality, especially for those in severe stages. The data from drug misuse clinics in Liverpool showed that difficult-to-reach groups could be reached, and colocated clinic points can be utilized to provide urgent and reliable health-care services to those who are hard to reach and lack access to conventional health care.[32,37] Since many of those patients are unaware of their conditions, the early detection and diagnosis of COPD can be helpful to prevent the fast decline in their lung condition [37].

CONCLUSION

The presented data suggest a correlation between heroin smoking and the onset of COPD. Heroin smokers showed a significant respiratory impairment compared to tobacco smokers of the same age group. Calling for COPD screening among heroin smokers who have a pulmonary disease history seems reasonable to identify COPD early.

Limitation

Although this study provides a glimpse of the long-term effects of heroin smoking, unfortunately, we were unable to track down the exact duration of heroin smoking for all heroin patients due to lack of transparency, some discrepancies in patients' self-reported files, and lack of adherence among users. We made a rough estimation based on the available information for regular smoking of heroin, which was averaged between 5 and 15 years. The vast majority of patients were chronic heroin smokers and have been diagnosed with COPD more than 5 years ago.

Availability of data and material

The raw data were obtained, recorded, and saved in English. The datasets obtained in Bahasa Malaysia, Mandarin, Tamil, or any other languages were transcribed and translated into English. The data were not publicly available as it contains information that could compromises research participants' privacy/consent. Therefore, the datasets analyzed for this paper will be assessed from the corresponding author upon reasonable request and approval from relevant authorities.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.