Low back pain (LBP) is a common musculoskeletal disorder experienced by adults of all ages (1). In the US, more than 55% of adults report back pain in the past year (2). LBP is the primary cause of restricted activity, sickness absence, loss of work productivity and reduced quality of life worldwide, resulting in high healthcare costs for individuals, families, and society (3). Chronic low back pain (CLBP) accounts for a majority of the dysfunction and expenses associated with LBP. The annual total direct cost per patient with CLBP in the US is $8,386 (4). Studies have shown that exercise can relieve LBP (5–7). The risk factors for LBP are multifactorial, including hereditary factors, physical risk factors (such as gender, age and history of a back injury), psychological factors (such as long-term mental stress, anxiety and fear of activities that indicate bodily harm or pain) and unhealthy lifestyle (such as alcohol drinking and smoking) (8, 9).

Recently, the interrelationships between pain, cigarette and smoking have received considerable attention because of their prevalence, public health consequences and serious comorbidities (10). More than two-thirds of Americans with chronic pain support lifelong nicotine use (11). People with chronic pain likely smoke more than the general population (12). Furthermore, recent estimates suggest that nearly 60% of people who are addicted to tobacco meet the criteria for chronic pain (13). Previous research has shown that smokers and those who have quit smoking tend to experience more widespread and severe pain than non-smokers (14).

Smoking has been linked to headaches, trunk pain and pain in the extremities (15, 16). Despite the increased likelihood of generalized pain, studies have found a strong relationship between spinal pain and smoking (16). Current and previous heavy smoking are associated with the amount and intensity of pain sites, that is, heavy smokers have a higher chance of having more pain sites and greater pain intensity than non-smokers (14). However, research on the association between smoking and pain intensity, function, depression and fear in patients with CLBP remains limited, particularly in studies that have conducted detailed comparisons of disease activity and functional status in smoking and non-smoking patients with CLBP. This study aims to investigate the interrelationship between smoking and CLBP from multiple dimensions such as pain intensity, psychology and quality of life. In addition, this study will investigate whether the amount of cigarettes smoked daily affects the pain intensity, dysfunction, anxiety and depression degree of patients with CLBP.

This study examined the association between smoking and pain, dysfunction, depression, anxiety and quality of life in patients with CLBP. We found significant differences in VAS, ODI, RMDQ and FABQ between smokers and non-smokers, which indicated that the smoking group had higher pain intensity, degree of dysfunction and fear-avoidance caused by CLBP than the non-smoking group. In addition, a correlation was observed between the daily cigarette smoking amount and pain, depression and fear belief in patients with CLBP.

The differences in pain and functional impairment between the smoking and non-smoking groups were statistically and clinically significant. VAS_max of the smoking group was concentrated at 5–7, whereas the non-smoking group was concentrated at 4–6. Therefore, patients with CLBP in the smoking group had severe pain, whereas the other group had mostly moderate pain (23). The clinical significance of the difference in ODI and RMDQ is significant. Patients in the smoking group likely have moderate disabilities, and they experienced more pain and difficulty sitting, lifting and standing (24). Patients in the non-smoking group had a mostly minimal disability, and they can cope with most living activities. However, no correlation was found between the daily cigarette smoking amount and ODI and RMDQ, indicating that the impact of smoking on the function of patients with CLBP can occur under slight smoking intensity and cannot necessarily aggravate with the increase of the amount of cigarettes smoked. The extent of the damage may be associated with the initiation and duration of smoking or the daily cigarette smoking amount at a particular stage in the evolution of the disease.

Regarding the association between smoking and pain, the results are consistent with previous studies (25). Smoking has been confirmed as a potential cause of musculoskeletal pain, and it is closely related to back pain (16). However, the mechanisms of LBP are only partly known. Smoking can increase the frequency of coughing, and coughing increases abdominal pressure, which intensifies the compression and stretch of the intervertebral disc on the nerve root, thereby blocking the venous return of the inflamed nerve root and increasing edema and sensitivity of the nerve to pain (26). Smoking is also associated with osteoporosis, which may alter the microscopic structure of the spine by reducing bone mineral content (27). It can impair fibrinolysis and increase fibrous deposition and scarring, leading to chronic infection and LBP (28). Moreover, smoking can reduce vertebral blood flow and affect intervertebral metabolic balance, thereby accelerating the degenerative process and making the spine more vulnerable to mechanical deformation and trauma (29–31). And it also reduces arterial blood flow, leading to ischemia of compressed nerve roots and pain. Furthermore, smoking alters disc gene expression, reduces collagen genes and increases proteoglycan and metalloproteinase 1 tissue inhibitory activity (32).

The amount of cigarettes smoked daily was correlated with VAS_max but not with VAS_min. This result may indicate that the extent to which smoking affects chronic pain is related to its basic pain intensity. For slight pain conditions, the role of smoking as an influencing factor was not prominent. However, as the pain got worse, the association between smoking and pain also increased. Thus, this study may provide new insights into the mechanism of the association between smoking and pain. Later studies investigating the relationship and mechanism of smoking and pain can focus on further quantifying pain intensity and determining whether a non-linear correlation exists between smoking and pain intensity, that is, the greater the intensity of pain, the greater the association between cigarette smoking and pain intensity.

The performance of the two groups on the one-leg standing test was consistent with their pain intensity differences. CLBP reduces the stability of the spinal area and increases the activation time of the gluteus medius muscle, which leads to differences in the ability to control lower limb balance (33). Smoking may affect the ability of patients with CLBP to stand on a single leg by affecting their pain intensity. However, at present, no relevant research has been conducted to determine whether or not smoking directly affects the neural mechanism controlling muscle coordination, which may be the direction of future research.

This study also found that after adjusting for age, income, education level, history of LBP, frequency of LBP last month and other confounders, the daily cigarette smoking amount remained positively correlated with the SDS, which indicated the relationship between the amount of cigarettes smoked daily and the aggravation of depressive symptoms in patients with CLBP. The current study found that depression was correlated with smoking (34). Chronic pain reduces social connection, and smokers are less socially active and lonelier than non-smokers (35). Vogt et al. (36) adjusted for income, education level, occupation, employment, life stress, childhood adversity, divorce and neurosis and found that smoking remained associated with depression. Research suggests that the smoking–depression association is bipolar. The presence of depressive symptoms increases the risk of developing nicotine dependence in smokers, thereby increasing the risk of depression (37). The occurrence of smoking addiction and depressive symptoms has a common neurotransmitter pathway, and they may have a common genetic material basis (38).

Anxiety and depression have been associated with a bidirectional effect of promoting smoking (39), and negative emotions have been confirmed as a central mechanism for the correlation of pain with smoking (40, 41). Pain-related anxiety was relevant to increasing pain intensity and positively related to heavy smoking and nicotine use to cope with aversive states (42). Increasing pain-related anxiety and pain sensitivity were related to early initiation of smoking (43). Whether or not smoking had a significant effect on the anxiety of patients with CLBP was not shown in this study probably because anxiety caused by the pain intensity of CLBP was not enough to cause the related effect of smoking, or the negative emotions caused by CLBP were more prone to depression. Future treatments should target whether CLBP-related anxiety may contribute to behavioural tendencies to relieve pain and negative effects through cigarette smoking.

CLBP can be attributed to a biological–psychological–social phenomenon. Patient’s anatomical injury factors interact with psychosocial factors (44), such as fear-avoidance belief, which indicates that some patients with LBP have negative beliefs about pain that can lead to a catastrophic psychological reaction, causing the patient to fear activities that may aggravate pain or injury. Avoidance of such activities can reduce the likelihood of repeat pain or injury (45). Fear-avoidance beliefs can be a predictor of outcome in patients with subacute LBP (46). In this study, the daily cigarette smoking amount was found to be positively correlated with FABQ_total and FABQ-W, particularly to work, which in turn led to excessive fear of pain or injury and gradually extended to fear of physical movement. This finding is also consistent with the association between smoking and pain intensity and depression in this study. Depression is an important influencing factor of fear-avoidance beliefs (47). Considering that depressed patients are often in a state of low emotional responsiveness and lack of enthusiasm and motivation to actively respond to symptoms, they tend to develop fear-avoidance beliefs about pain. Depression, including clinically diagnosed depression and patient-reported depressive symptoms, is common in patients with CLBP (48). Pain patients with depressive symptoms tend to have more intense pain experiences and more severe physical damage. Smoking is closely related to depression (37), indicating that smoking may be related to fear beliefs by affecting depressive symptoms in patients with CLBP. Future research can focus on the interaction of smoking, depression and fear-avoidance beliefs in patients with CLBP.

The daily cigarette smoking amount is related to the impact of LBP on work but not related to the impact of LBP on life probably because the working conditions of most people are relatively monotonous, which reduces the impact of other factors to a higher degree, thereby making the impact of smoking fully exposed. In daily life, individuals have more options to maintain low-intensity LBP for themselves, which highlight the weight of factors such as income, leisure time and daily activity in the impact of LBP on life and indirectly offset the effect of the amount of cigarettes smoked daily. This result indicates that future research should include more population in the study to explore the correlation between smoking and the impact of LBP on life under more undisturbed conditions.