
==== Front
Medicine (Baltimore)
Medicine (Baltimore)
MD
Medicine
0025-7974
1536-5964
Lippincott Williams & Wilkins Hagerstown, MD

39312320
MD-D-24-01448
00021
10.1097/MD.0000000000039705
3
3400
Research Article
Observational Study
A cross-sectional study of the association between blood cadmium and mortality among adults with myocardial infarction
Li Ren-jie MD jiqxiang@163.com
a
https://orcid.org/0000-0003-4315-6649
Wen Ying-xu BD b*
a Emergency Department, Affiliated Hospital of Putian University, Putian, Fujian, China
b Emergency Department, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China.
* Correspondence: Ying-xu Wen, Emergency Department, The Second Affiliated Hospital of Hainan Medical University, Longhua District, Haikou 570000, Hainan, China (e-mail: wenyingxu570806@163.com).
20 9 2024
20 9 2024
103 38 e3970505 2 2024
23 5 2024
23 8 2024
Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.
2024
https://creativecommons.org/licenses/by-nc/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal.

Cadmium (Cd) plays a key role in the occurrence of myocardial infarction (MI). We aimed to explore the association between blood Cd levels and all-cause mortality of MI on the basis of the National Health and Nutrition Examination Survey databases. This study included 800 adults with MI to obtain blood Cd concentrations and their follow-up information. The association between Cd concentrations and mortality was analyzed using Cox regression, restricted cubic spline (RCS) models, mediation analysis, receiver operating characteristic curve, and Kaplan–Meier curves. All the patients were divided into 4 groups according to the quartiles of blood Cd levels (Q1, Q2, Q3, and Q4). Cox regression analysis with adjustment for covariates indicated that Cd was the promoting factor of mortality, and patients with higher Cd had a higher death risk. The RCS model indicated an “inverted checkmark” shaped correlation between Cd levels and mortality, and a turning point of 1.06 μg/L was found. A significant positive correlation was observed on the left of the turning point. Grouped patients by turning point into 2 groups, Kaplan–Meier analysis showed that the low-concentration group had a lower death risk than the high-concentration group. Subgroup analysis revealed that the prognostic effect of Cd was more pronounced in patients with former smoking history, and receiver operating characteristic curve showed that blood Cd had a better-predicting function in patients with MI. Blood Cd levels were significantly related to all-cause mortality in patients with MI, especially in patients with Cd < 1.06 μg/L.

blood cadmium level
correlation
cross-sectional study
mortality of myocardial infarction
NHANES
OPEN-ACCESSTRUE
==== Body
pmc1. Introduction

Heavy metal contamination is a serious global environmental problem.[1] It can enter the circulatory system through the digestive tract, respiratory tract, or skin, accumulating in various organs.[2] Upon reaching a certain level, it can cause damage to the endocrine, cardiovascular, and nervous systems.[3–5] Cadmium (Cd), a common heavy metal, is nonessential for people. It is an underlay risk to human health via the food chain and something containing Cd, for example, the battery industry, tobacco, electroplating manufacturing, and pigments.[6,7] In addition, the stability and permeability of Cd led to its persistence and accumulation in the body, and the biological half-life in the body was as long as 10−30 years.[8] Most published studies have shown that Cd exposure can result in toxic effects on various organs and affect many human diseases including diabetes,[9] bronchitis,[10] and cardiovascular disease.[11]

Myocardial infarction (MI) is one of the most serious cardiovascular diseases, with high morbidity and mortality rates worldwide.[12] Previous studies found that environmental Cd exposure was 1 influencing factor in the occurrence of because peripheral blood vessels were an important target for cadmium accumulation and action MI.[13] However, the effect of Cd on MI was controversial and limited because it was generally classified as a cardiovascular disease. Some research indicated that cadmium was a predictive risk factor for cardiovascular disease and that the relationship between them was influenced by other factors such as gender, smoking, and other diseases.[14–16]

Previous studies have reported the relationship between Cd and MI risk, but the correlation between Cd exposure and mortality among patients with MI was unclear. Therefore, this study aimed to explore the relationship between blood Cd levels and mortality in participants with MI. Blood Cd levels were an important marker for assessing long-term exposure to Cd in individuals. We extracted blood Cd levels from the National Health and Nutrition Examination Survey (NHANES) of participants with MI. The effects were analyzed using Cox regression models, RCS models, and Kaplan–Meier (KM) curves, receiver operating characteristic (ROC) curves to provide new insights into therapeutic interventions for MI and a basis for subsequent in-depth studies.

2. Materials and methods

2.1. Participants and Procedures

This work used data from the NHANES database (NHANES https://www.cdc.gov/nchs/nhanes/, 2007−2008, 2009−2010, 2011−2012, 2013−2014, 2015−2016, 2017−2018) participants. The database is a periodic survey of a representative sample of the civilian noninstitutionalized US population, including individual-level food intake, health behaviors, health status, and sociodemographics, and is designed by the organization of the National Center of Health Statistics at the Centers for Disease Control and Prevention. In addition, the database is public for researchers, and some details about it are available on its website.[17]

In our work, we combined data from the 2007 to 2018 NHANES database. We excluded participants aged < 20 years and did not answer the research problem. Then, we considered a participant to have an MI when he or she answered “yes” to the question ‘ Has your doctor ever told you that you had a heart attack/MI? ‘.[18] To further select the participants of this study, we excluded those who missed covariates. A total of 800 participants with MI were included in this work. Figure 1 shows the flowchart of the study.

Figure 1. The flowchart of the study. BMI = body mass index, NHANES = National Health and Nutrition Examination Survey.

2.2. Measurement of blood Cd concentration

Cd was measured in whole blood using multi-element atomic absorption spectrometry (PerkinElmer model SIMAA 6000), with Zeeman background correction on the basis of the NHANES website. Details of NHANES laboratory procedures were described based on reported literature.[19–21]

2.3. Mortality outcome

We collected the all-cause mortality and follow-up time from the National Death Index mortality database of NHANES. The “all-cause mortality statute” variable name is “mortstat” and the variable name of follow-up time is “permth_exm” in the Death Index mortality database.

2.4. Other participants’ characteristics

Characteristics including age, sex, race, body mass index (BMI), smoking status, education, annual family income, family poverty income ratio, and alcohol use were acquired from the in-person interviews. Moreover, we categorized race as White, Black, Mexican American, and others (this included NH Asian Hispanic, and other or multiracial). Education attainment was classified into 5 levels including less than 9th grade, 9−11 grade, high school grade, some college or AA degree, and college graduate or above.

Annual family income was classified into 3 levels including greater than USD75,000, USD20,000–75,000, and <USD20,000. Marital status includes never married, married, separated, widowed, divorced, or living with a partner. Hypertension was defined on the basis of previous doctor diagnosis, taking prescribed medicine to decrease blood pressure (BP), and BP of ≥ 140/90 mm Hg. Smoker was defined as adults who smoked >100 cigarettes in life and smoked some days or every day. Smokers who do not currently smoke cigarettes were considered former smokers. Never-smoker was defined as adults who smoked <100 cigarettes in life. We categorized alcohol use as never (had < 12 drinks in a lifetime), former (had ≥ 12 drinks in 1 year and did not drink last year, or did not drink last year but drank ≥ 12 drinks in lifetime), mild (1 is for female and 2 is for male), moderate (2 is for female and 3 is for male; or binge ≥ 2 and binge < 5), heavy (3 is for female and 4 is for male; or binge ≥ 5) based on the previous studies.[22,23] Daily energy intake was collected from the dietary data, and total cholesterol content was collected from the laboratory data.

2.5. Statistical analyses

Participants’ characteristics were divided into 4 groups compared and based on the quartiles of blood Cd concentration (Q1, Q2, Q3, and Q4). Categorical variables were expressed as frequencies and percentages, while continuous variables were reported as mean ± SD. Subsequently, the difference between groups was compared using ANOVA for continuous variables, whereas the chi-square test was used to compare the categorical variables.

The dietary day 1 sample weight (WTDRD1/6) was used for weighted analyses (https://wwwn.cdc.gov/nchs/nhanes/tutorials/default.aspx) to improve the accuracy of statistical analysis. The weighted Cox regression was used to explore the association and hazard ratios (HRs) and 95% confidence intervals between all-cause mortality and blood Cd level. To rule out the confounding factors, we adjusted for race, age, sex, mar, and annual family income in model 1; model 2 was adjusted for model 1 plus BMI, smoke, and daily energy intake; model 3 was adjusted for model 2 plus hypertension, alcohol, total cholesterol content. Subgroup analysis was performed by weighted Cox regression stratified by race, sex, annual family income, smoking, alcohol, and hypertension. The effects of age and blood Cd level on the morality of patients with MI were specifically explored via the weighted Cox regression analysis. We tested for interaction using models adjusted for variables with the addition of interaction terms between the main effect variable and subgroup. The restricted cubic spline models were used for the nonlinear analysis. Mediation analysis was used to explore the relationship between the follow-up time and key factors. All the analyses were performed using IBM SPSS 23.0 software and R software 3.6. Additionally, P value < 0.05 was considered as statistically significant.

3. Results

3.1. Participants’ baseline characteristics by blood Cd concentration

Table 1 summarizes baseline participants’ characteristics by blood Cd concentration and mortality. A total of 800 participants with MI were enrolled, and among them 31.38% were female. The age, daily energy intake, follow-up time, BMI, family poverty income ratio, sex, race, annual family income, smoking, education level, marital status, and alcohol were significantly different among the 4 groups. Total cholesterol content and hypertension were not significantly different among the 4 groups.

Table 1 The variable of MI patients according to the blood Cd concentration.

Variable	Blood Cd levels (μg/L)	P value	
Q1
n = 209	Q2
n = 178	Q3
n = 206	Q4
n = 207	
Age	63.69 (0.81)	68.89 (0.92)	65.71 (1.07)	60.47 (0.95)	<0.01	
Daily energy intake (kcal/d)	2171.38 (88.36)	1783.43 (75.75)	1843.54 (67.68)	1944.23 (81.29)	<0.01	
Follow-up time (mo)	73.77 (4.18)	78.77 (3.93)	81.21 (4.23)	72.90 (3.58)	0.22	
Total cholesterol content (mg/dL)	171.17 (4.24)	172.97 (4.78)	181.98 (3.87)	180.34 (3.25)	0.20	
BMI	32.98 (0.61)	31.34 (0.54)	30.16 (0.60)	29.32 (0.66)	<0.01	
Family poverty income ratio	3.19 (0.16)	2.81 (0.13)	2.58 (0.18)	1.97 (0.14)	<0.01	
Sex (%)					0.03	
 Female	52 (24.84)	56 (33.47)	74 (42.87)	69 (37.29)		
 Male	157 (75.16)	122 (66.53)	132 (57.13)	138 (62.71)		
Race (%)					0.02	
 Black	16 (3.42)	18 (5.59)	19 (4.53)	30 (8.24)		
 Mexican American	17 (3.68)	8 (2.14)	8 (2.21)	2 (0.23)		
 Other	105 (39.22)	102 (48.98)	121 (47.21)	124 (52.30)		
 White	71 (53.67)	50 (43.29)	58 (46.05)	51 (39.23)		
Annual family income (%)					< 0.01	
 Less than USD 20,000	59 (15.07)	52 (22.04)	91 (29.07)	104 (43.00)		
 USD 20,000–75,000	107 (49.92)	98 (61.66)	88 (42.85)	87 (44.59)		
 Greater than USD 75,000	43 (35.01)	28 (16.30)	27 (28.08)	16 (12.41)		
Smoke (%)					<0.01	
 Never	116 (56.87)	78 (40.62)	68 (34.00)	6 (1.89)		
 Former	88 (41.81)	94 (55.19)	91 (46.49)	53 (22.85)		
 Now	5 (1.32)	6 (4.19)	47 (19.51)	148 (75.26)		
Hypertension (%)					0.95	
 No	51 (22.65)	34 (21.71)	41 (25.05)	45 (23.87)		
 Yes	158 (77.35)	144 (78.29)	165 (74.95)	162 (76.13)		
Education level (%)					<0.01	
 Less than 9th grade	36 (8.15)	32 (10.22)	34 (9.27)	27 (8.98)		
 9–11	17 (2.94)	21 (10.10)	38 (15.11)	54 (27.96)		
 High school grade	47 (27.09)	48 (35.02)	55 (27.23)	55 (29.08)		
 Some college or AA degree	65 (36.44)	47 (24.11)	44 (25.21)	52 (25.67)		
 College graduate or above	44 (25.38)	30 (20.55)	35 (23.17)	19 (8.30)		
Marital status (%)					<0.01	
 Never married	11 (3.40)	10 (5.99)	16 (7.18)	19 (8.37)		
 Married	121 (65.26)	113 (64.63)	97 (55.97)	84 (41.41)		
 Separated	5 (0.99)	3 (1.43)	10 (4.05)	4 (2.14)		
 Widowed	32 (15.57)	35 (18.26)	38 (13.18)	36 (15.53)		
 Divorced	32 (9.71)	13 (7.59)	37 (15.71)	40 (14.26)		
 Living with partner	8 (5.07)	4 (2.10)	8 (3.90)	24 (18.29)		
Alcohol (%)					0.03	
 Former	60 (22.52)	55 (31.49)	64 (30.16)	66 (27.98)		
 Mild	86 (49.12)	76 (43.79)	69 (36.76)	69 (35.75)		
 Moderate	20 (10.36)	12 (5.84)	21 (11.62)	18 (8.36)		
 Never	21 (8.17)	25 (12.65)	27 (9.47)	12 (3.96)		
 Heavy	22 (9.84)	10 (6.23)	25 (12.01)	42 (23.95)		
BMI = body mass index, MI = myocardial infarction.

3.2. Blood Cd concentration and mortality

The association between the blood Cd concentration and mortality is presented in Table 2. Among the participants with MI, the dead were 266. The Cox regression analysis showed that the blood Cd concentration was the promoting factor of all-cause mortality (hazard ratio > 1). After adjusting for some variables including age, daily energy intake, follow-up time, BMI, family poverty income ratio, sex, race, annual family income, smoking, education level, marital status, alcohol, total cholesterol content, and hypertension, we found that the all-cause mortality of the participants with MI was increasing with the increasing of the blood Cd concentration (all P value for trend < 0.05, Table 2).

Table 2 The HR (95% CIs) for all-cause mortality according to blood Cd concentration.

Blood Cd levels (μg/L)	Crude model	Model 1	Model 2	Model 3	
HR (95% CI)	P	95% CI	P	HR (95% CI)	P	HR (95% CI)	P	
Q1	Ref		Ref		Ref		Ref		
Q2	1.79 (1.06–3.04)	0.03	1.25 (0.75–2.08)	0.39	1.20 (0.73–1.99)	0.48	1.24 (0.75–2.06)	0.41	
Q3	1.87 (1.22–2.87)	<0.01	1.46 (0.98–2.19)	0.07	1.40 (0.90–2.16)	0.13	1.38 (0.90–2.10)	0.14	
Q4	2.25 (1.46–3.47)	<0.01	2.51 (1.57–4.01)	<0.01	2.37 (1.27–4.42)	0.01	2.30 (1.24–4.26)	0.01	
P for trend		<0.01		<0.01		0.02		0.02	
Crude model: blood Cd concentration. Model 1: blood Cd concentration eth, age, sex, mar, annual family income. Model 2: blood Cd concentration eth, age, sex, mar, annual family income, BMI, smoke, daily energy intake. Model 3: blood Cd concentration eth, age, sex, mar, annual family income, BMI, smoke, daily energy intake, hypertension, alcohol, total cholesterol content.

CI = confidence intervals, HR = hazard ratio.

To explore the detailed relationship between the blood Cd concentration and mortality, the restricted cubic spline analysis was performed in this work. The results showed that the relationship between the 2 is similar to the “inverted checkmark.” In addition, we acquired 1 turning point (blood Cd concentration was 1.06 μg/L) from the “inverted checkmark” shape. When the blood Cd concentration was <1.06 μg/L, there was an upturn trend in the risk of death as the blood Cd concentration increased. However, there was a slight downward trend in the risk of death as the concentration increased above 1.06 μg/L (Fig. 2A). We speculated that the insignificant effect of Cd may be related to age. Generally, the advanced age always plays a more important role in the death risk of populations than other variables. Therefore, we further detailedly explored the correlation of age and Cd with the death risk on the left and right of the turning point. Cox regression analysis showed that among patients with Cd < 1.06 μg/L, the hazard ratio of Cd was higher than that of Cd both in univariate (2.33 vs 1.08) and multivariate (2.54 vs 1.07) analyses. While in patients with Cd ≥ 1.06 μg/L, we only found a significant correlation between higher age and death risk (all P < .05). These results indicated that among patients with Cd ≥ 1.06 μg/L, the death risk may be mainly related to the increased age rather than the Cd (Table 3).

Table 3 Univariate and multivariate Cox regression analysis of the all-cause mortality on blood Cd concentration and age.

Group	Cox	Subject	P value	HR	Lower	Upper	
Cd ≥ 1.06 μg/L	Univariate	Blood Cd concentration	0.24	0.82	0.59	1.14	
		Age	<0.01	1.07	1.04	1.09	
	Multivariate	Blood Cd concentration	0.92	0.99	0.74	1.32	
		Age	<0.01	1.07	1.04	1.09	
Cd < 1.06 μg/L	Univariate	Blood Cd concentration	<0.01	2.5	1.42	4.52	
		age	<0.01	1.08	1.06	1.10	
	Multivariate	Blood Cd concentration	<0.01	2.33	1.27	4.23	
		Age	<0.01	1.07	1.06	1.09	
HR = hazard ratio.

Figure 2. The correlation analysis between blood Cd level and all-cause mortality in patients with MI. (A) The RCS analysis. (B) The KM survival analysis. KM = Kaplan–Meier, MI = myocardial infarction, RCS = restricted cubic spline.

In addition, we analyzed the correlation between Cd and survival time. The participants with MI were grouped into 2 groups based on the turning point of blood Cd concentration. The KM plot was established and showed that the low-concentration group had a lower risk of all-cause mortality than the high-concentration group (Fig. 2B).

3.3. Subgroup analysis of all-cause mortality

We performed a subgroup analysis to find the precise participants for this turning point of blood Cd concentration via Cox regression analysis. Meanwhile, the interaction analysis was also conducted between the blood Cd concentration and other factors for all-cause mortality. The results of the subgroup analysis showed that there was a significant association between participants with MI who had the characteristics as following: former smokers, male, never smoked or without hypertension (P < .05), and all-cause mortality. The interaction analysis results indicated that there was an interaction between the blood Cd concentration and smoking for all-cause mortality (P value for interaction < 0.05, Table 4). Then, we also found that smoking did not function between the all-cause mortality and smoking via mediation analysis (Table 5). The subgroup KM survival analysis showed that low blood Cd concentrations were more beneficial in MI patients with former smoking with significantly different (P < .05, Figure 3A). However, there was low blood Cd concentrations were related to all-cause mortality in male MI patients, never smoking MI patients, or MI patients without hypertension with not significantly different (Fig. 3B, 3C, and D). The ROC analysis was used to test the efficiency of blood Cd concentration in predicting all-cause mortality for all patients with MI (Fig. 4A) and these patients with former smoking history (Fig. 4B). The results indicated that blood Cd had a better function for predicting the survival of patients.

Table 4 Cox regression and interaction analysis for all-cause mortality according to the subgroups.

Characters	HR (95% CI)	P	P for interaction	
Race			0.23	
 White	0.86 (0.60–1.23)	0.41		
 Black	1.36 (0.90–2.06)	0.15		
 Mexican American	2.59 (0.26–26.03)	0.42		
 Other	1.17 (0.03–1.32)	0.05		
Sex			0.05	
 Female	1.02 (0.84–1.23)	0.85		
 Male	1.31 (1.06–1.62)	0.01		
Annual family income			0.17	
 Less than USD 20,000	0.97 (0.81–1.16)	0.76		
 USD 20,000–75,000	1.13 (0.84–1.51)	0.42		
 Greater than USD 75,000	2.88 (0.82–10.14)	0.10		
Smoke			<0.01	
 Never	4.90 (1.59–15.06)	0.01		
 Former	3.98 (1.76–9.01)	<0.01		
 Now	1.00 (0.78–1.27)	0.97		
Alcohol			0.79	
 Never	1.14 (0.54–2.41)	0.74		
 Former	1.22 (0.83–1.78)	0.31		
 Mild	1.39 (0.96–2.00)	0.08		
 Moderate	1.72 (0.94–3.15)	0.08		
 Heavy	1.10 (0.97–1.23)	0.13		
Hypertension			0.32	
 No	1.20 (1.06–1.36)	<0.01		
 Yes	1.06 (0.86–1.31)	0.59		
HR = hazard ratio.

Table 5 Mediation analysis between the all-cause mortality, blood Cd concentration, and smoking.

Path	Coef	SE	CI (2.5%)	CI (97.5%)	P	
Survival time~smoking	0.63	0.03	0.57	0.70	<0.01	
Smoking~survival time	0.02	0.02	−0.02	0.06	0.40	
Total	0.07	0.03	0.02	0.12	<0.01	
Direct	0.09	0.03	0.03	0.14	<0.01	
Indirect	0.02	0.02	−0.05	0.02	0.39	
CI = confidence interval.

Figure 3. The KM survival curve was used to explore the relationship between Cd level and all-cause mortality based on the subgroups. (A) Former smoking; (B) male; (C) never smoking; (D) without hypertension. HR = hazard ratio, KM = Kaplan–Meier.

Figure 4. The ROC curve analyses were used to analyze the performance of Cd level for predicting the death risk of patients. (A) All of the populations. (B) The former smoking subgroup. AUC = area under the curve, ROC = receiver operating characteristic.

4. Discussion

In the present study, we found that the blood Cd level was significantly related to the all-cause mortality of the patients with MI. There is a nonlinear relationship between them. Specifically, the death risk of patients with MI increased with the increase of the blood Cd when it was <1.06 μg/L, while the death risk of patients with MI decreased with the increase of the blood Cd when it was in the range of 1.06−3.00 μg/L. The finding worthy of our attention was that the smoking had an interaction function, which affected the relationship between the blood Cd level and the all-cause mortality of the patients with MI.

In nearly ten years, many reported researches indicated that chronic low-concentration Cd exposure increases the incidence of cardiovascular and cerebrovascular diseases, resulting in increased all-cause mortality and cardiovascular and cerebrovascular mortality.[24,25] This is in line with our finding that blood Cd levels in a certain range had a positive relationship with mortality of the patients with MI. We found the all-cause mortality risk was decreased with the blood Cd level when the blood Cd level was >1.06 μg/L. We hypothesize that the effect of age on mortality covers the risk of blood Cd levels on mortality when the blood Cd level was more than 1.06 μg/L. Then, the Cox regression analysis verified our hypothesis. Among patients with Cd ≥ 1.06 μg/L, the more important risk factor was the increased age rather than the Cd.

As we know, MI is a complex pathophysiological process involving multiple factors. Coronary atherosclerosis and plaque formation are the pathological basis of MI. Plaque erosion or damage associated with thrombosis, resulting in high stenosis or complete occlusion of the vascular lumen is a key chain in the pathogenesis of acute MI.[26,27] Peripheral blood vessels are also the target organs for Cd accumulation. Vascular endothelial cells are in direct contact with Cd in blood and vessel wall, which is an important target of Cd action. Therefore, the direct contact of vascular endothelial cells with Cd accumulated in blood circulation and vascular wall is the direct target of Cd toxicity, which was been proved by in vivo experiments in mice.[28] Recent studies by researchers have shown that Cd stimulation can also activate the expression of ERG in endothelial cells, thereby enhancing the binding of ERG to the 56ETS site on the von Willebrand factor (vWF) gene promoter and promoting the transcription and expression of vWF gene.[29] ERG mediates the differentiation of embryonic stem/progenitor cells into endothelial cells by activating the transcription of endothelial cell-specific markers vWF, recognized as a specific molecular biological marker reflecting the status of vascular endothelial function,[30] which is necessary for endothelial cell lineage, angiogenesis, and angiogenesis, and regulates cell survival, permeability, and cytoskeleton dynamics.[31,32] Summarizing, blood Cd level had a positive relationship with mortality in the patients with MI, which also was affected by age when it was more than the threshold value.

Smoking is one of the main ways of Cd exposure in nonoccupational population.[33] A reported study found that the concentration of Cd in the plasma of the general population was 10−100 nM. The concentration of Cd in the intima of the arterial wall of the smokers was about 1.5 μM, while the concentration of Cd in the aortic wall of the heavy smokers can be as high as 20 μM. Smoking is 1 risk factor for patients with MI, and the plasma vWF level in smokers was higher than that in nonsmokers.[34,35] Barregard et al[36] found increased mortality risk among never smokers following Cd exposure in a large population-based cohort study of Swedish individuals. Eric et al[37] indicated that the relationship between Cd exposure and the prevalence of cardiovascular disease is not different in an individual’s smoking state. However, our data indicated that smoking affected the relationship between the blood Cd and the all-cause mortality of the patients with MI. This may be because the definition of smoking and the categorization criteria of smoking were different in different researches.

There were some limitations in this work. First, the participants were collected from the NHANES database who only represented Americans. Second, the specific occurrence time of Cd exposure and MI could not be determined due to the cross-sectional research. Third, whether the blood Cd concentration can represent the level of Cd exposure is a question worth considering. However, our research was important for predicting the mortality of MI patients when did not consider these shortcomings.

5. Conclusion

Few studies reported a detailed association between Cd level and mortality in patients with MI currently. Our results preliminary demonstrated that blood Cd levels were positive with the all-cause mortality when it is <1.06 μg/L while were negative with the all-cause mortality when it is >1.06 μg/L in patients with MI. In addition, there was an interaction function between the blood Cd level and smoking in increasing the all-cause mortality risk. These results suggest that we should strengthen environmental protection, reduce heavy metal exposure, and reduce the harm to MI patients.

Author contributions

Conceptualization: Ren-jie Li.

Data curation: Ren-jie Li.

Formal analysis: Ren-jie Li.

Writing – original draft: Ren-jie Li.

Investigation: Ying-xu Wen.

Methodology: Ying-xu Wen.

Supervision: Ying-xu Wen.

Writing – review and editing: Ying-xu Wen.

Abbreviations:

BMI body mass index

Cd Cadmium

KM Kaplan–Meier

MI myocardial infarction

NHANES National Health and Nutrition Examination Survey

RCS restricted cubic spline

ROC receiver operating characteristic.

The authors have no funding and conflicts of interest to disclose.

The Ethics Committee of Affiliated Hospital of Putian University deemed that this research is based on open-source data, so the need for ethics approval was waived.

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

How to cite this article: Li R-j, Wen Y-x. A cross-sectional study of the association between blood cadmium and mortality among adults with myocardial infarction. Medicine 2024;103:38(e39705).
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